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外文医学文献导读(三十八):《细胞周期蛋白在子宫肿瘤中的表达》
2020-09-30 08:23     (点击: )
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本次专题的检索年限:2018-2020  

检索式: Uterine Neoplasms AND Cyclin

使用的数据库:PubMedFMRS

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编号:1

题名:ESRP1 Induces Cervical Cancer Cell G1-Phase Arrest Via Regulating Cyclin A2 mRNA Stability.

ESRP1通过调节细胞周期蛋白A2 mRNA稳定性诱导宫颈癌细胞G1期停滞

作者:Chen, ZH;Jing, YJ;Yu, JB;Jin, ZS;Li, Z;He, TT;Su, XZ

出处:Int J Mol Sci.2019,20(15):

IF4.556

摘要:  Accumulating evidence indicates that epithelial splicing regulatory protein 1 (ESRP1) can inhibit the epithelial-to-mesenchymal transition (EMT), thus playing a central role in regulating the metastatic progression of tumors. However, it is still not clear whether ESRP1 directly influences the cell cycle, or what the possible underlying molecular mechanisms are. In this study, we showed that ESRP1 protein levels were significantly correlated with the Ki-67 proliferative index (r = -0.521; p < 0.01), and that ESRP1 overexpression can significantly inhibit cervical carcinoma cell proliferation and induced G1-phase arrest by downregulating cyclin A2 expression. Importantly, ESRP1 can bind to GGUGGU sequence in the 3'UTR of the cyclin A2 mRNA, and ESRP1 overexpression significantly decreases the stability of the cyclin A2 mRNA. In addition, our experimental results confirm that ESRP1 overexpression results in enhanced CDC20 expression, which is known to be responsible for cyclin A2 degradation. This study provides the first evidence that ESRP1 overexpression induces G1-phase cell cycle arrest via reducing the stability of the cyclin A2 mRNA, and inhibits cervical carcinoma cell proliferation. The findings suggest that the ESRP1/cyclin A2 regulatory axis may be essential as a regulator of cell proliferation, and may thus represent an attractive target for cervical cancer prevention and treatment.

主题词:Cyclin A2/genetics*/细胞周期蛋白A2/遗传学*

主题词:G1 Phase Cell Cycle Checkpoints/genetics*/G1期细胞周期检查点/遗传学*

主题词:Gene Expression Regulation, Neoplastic*/基因表达调控, 肿瘤*

主题词:RNA Stability*/RNA稳定性*

主题词:RNA-Binding Proteins/genetics*/RNA结合蛋白质类/遗传学*

主题词:Uterine Cervical Neoplasms/genetics*/宫颈肿瘤/遗传学*

全文链接:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6695732/

 

 

编号:2

题名:LncRNA CRNDE acts as an oncogene in cervical cancer through sponging miR-183 to regulate CCNB1 expression.

LncRNA CRNDE通过海绵化miR-183调节CCNB1表达而成为宫颈癌的致癌基因

作者:Bai, X;Wang, W;Zhao, P;Wen, J;Guo, X;Shen, T;Shen, J;Yang, X

出处:Carcinogenesis.2020,41(1):111-121

IF4.603

摘要:  Studies have identified a series of lncRNAs that contributed to various tumors, although the underlying mechanisms remain largely unclear. We proposed a ceRNA network and investigate relations among lncRNA/miRNA/mRNA in cervical cancer (CC). The genes of differential expression and lncRNA/miRNA/mRNA network were identified by combining TCGA, miRcode, starBase, miRTarBase, miRDB, TargetScan and STRING databases. Meanwhile, the function enrichment was recognized with Gene Ontology and Kyoto Encyclopedia of Genes and Genomes. Quantitative real time-PCR (qRT-PCR) was performed to determine colorectal neoplasia differentially expressed (CRNDE) expression in CC tissues and cell lines. The effects of CRNDE on the CC biological functions and cyclin B1 (CCNB1) expression were detected by conducting in vitro and in vivo experiments. Quantitative real time-PCR, western blot and dual-luciferase reporter assay were used to predict the target of miR-183. Furthermore, rescue experiments were conducted to further confirm the regulation of CCNB1 by CRNDE. Systematic analyses of bioinformatics from several databases predicted that CRNDE, miR-183 and CCNB1 were in the same network path. Their expressions were up-regulated in CC tissues and cells. Silencing CRNDE-inhibited cell proliferation, migration and invasion, restricted solid tumor growth and promoted cell apoptosis. Moreover, our results suggested that miR-183 targeted the CCNB1 3'UTR and regulated its expression. Additionally, miR-183 mimic could inverse the antitumor function of CRNDE inhibition and partially eliminated the attenuated expression of CCNB1 induced by silencing CRNDE, indicating that CRNDE could positively regulate CCNB1 expression by sponging miR-183. Our study highlighted a role for the CRNDE/miR-183/CCNB1-axis in CC and offered a promising diagnostic strategy for CC treatment.

主题词:Cyclin B1/genetics*/细胞周期蛋白B1/遗传学*

主题词:Gene Expression Regulation, Neoplastic*/基因表达调控, 肿瘤*

主题词:MicroRNAs/genetics*/RNAs/遗传学*

主题词:RNA, Long Noncoding/metabolism*/RNA, 长链非编码/代谢*

主题词:Uterine Cervical Neoplasms/genetics*/宫颈肿瘤/遗传学*

全文链接:请使用FMRS数据库下载该篇文章。

 

 

编号:3

题名:Overexpression of circular RNA hsa_circ_0001038 promotes cervical cancer cell progression by acting as a ceRNA for miR-337-3p to regulate cyclin-M3 and metastasis-associated in colon cancer 1 expression.

环状RNA hsa_circ_0001038的过表达通过充当miR-337-3pceRNA来调节细胞周期蛋白M3及其与结肠癌1表达的相关转移,从而促进宫颈癌细胞的发展

作者:Wang, Y;Wang, L;Wang, W;Guo, X

出处:Gene.2020,733 :144273

IF2.984

摘要:  Cervical cancer (CC) is a common cancer threatens women's health worldwide. Circular RNAs (circRNAs) is critically involved in carcinogenesis of various cancers. This work aimed to explore the expression pattern, functions and mechanisms of hsa_circ_0001038 in CC. RT-qPCR was performed to evaluate the levels of hsa_circ_0001038 in CC cell lines and tissues. Kaplan-Meier curves was applied to evaluate the overall survival rate of CC patients with high or low expression of hsa_circ_0001038. Fisher's exact test was analyzed to explore the relationship of hsa_circ_0001038 expression and CC patients' clinical features. Loss/Gain-of function assays were used to evaluate the role of hsa_circ_0001038 on the growth, apoptosis, migration and invasion of CC cell lines. The competing endogenous RNA (ceRNA) mechanism was predicted by bioinformatics databases and verified by dual-luciferase reporter assay. We found that hsa_circ_0001038 was highly expressed in CC cells and tissues and elevated hsa_circ_0001038 was closely related to the clinical severity including lymph node invasion and myometrial invasion. In addition, overexpressed hsa_circ_0001038 correlated with unfavorable outcome in CC patients. Knockdown of hsa_circ_0001038 attenuated cell growth, migration, and invasion but induced cell apoptosis. Ectopic expression of hsa_circ_0001038 increased cell oncogenic properties. For mechanism investigation, hsa_circ_0001038 could sponge miR-337-3p to release its suppression on cyclin-M3 (CNNM3) and metastasis-associated in colon cancer 1 (MACC1), thereby promoting CC cell growth and invasive potential, respectively. In conclusion, hsa_circ_0001038 plays an oncogenic role in CC cells partly by activating CNNM3 and MACC1.

主题词:Cyclins/metabolism/细胞周期蛋白类/代谢

主题词:Gene Expression Regulation, Neoplastic/genetics/基因表达调控, 肿瘤/遗传学

主题词:Transcription Factors/genetics/转录因子/遗传学

主题词:Uterine Cervical Neoplasms/genetics*/宫颈肿瘤/遗传学*

全文链接:请使用FMRS数据库下载该篇文章。

 

 

编号:4

题名:CRIP1 promotes cell migration, invasion and epithelial-mesenchymal transition of cervical cancer by activating the Wnt/β-catenin signaling pathway.

CRIP1通过激活Wnt /β-catenin信号通路来促进宫颈癌的细胞迁移,侵袭和上皮-间质转化

作者:Zhang, LZ;Huang, LY;Huang, AL;Liu, JX;Yang, F

出处:Life Sci.2018,207:420-427

IF3.448

摘要:  Cervical cancer (CC) is the third most common cancer and the fourth leading cause of malignancy-related mortality in women worldwide. In addition, epithelial-mesenchymal transition (EMT) has been generally studied in tumor metastasis researches in recent years. Cysteine-rich intestinal protein 1 (CRIP1) is differently expressed in human cancer cells. However, the role it plays in CC has not been revealed at present. Preliminary experiments have shown that CRIP1 had a higher expression in CC tissues, compared with adjacent noncancerous tissues. Real-time PCR and western blot were performed to analyze CRIP1 expression in CC cell lines. CRIP1 transient transfection vector and siRNA were constructed. Further analysis revealed the promotion effects of CRIP1 on the cell migration and invasion of CC in vitro (P<0.01). In addition, western blot was performed to show that CRIP1 mediates EMT by means of EMT marker detection. The expression of CRIP1 and β-catenin in CC tissues was analyzed by immunohistochemistry (IHC). Interestingly, CRIP1 and β-catenin were both highly expressed in CC tissues (P<0.01). Furthermore, CRIP1 increased the protein expression level of c-myc, cyclinD-1 and cytoplasmic β-catenin, which are indicators for activating the Wnt/β-catenin signaling pathway. In conclusion, CRIP1 promotes cell migration and invasion, mediates EMT and activates the Wnt/β-catenin signaling pathway in CC.

主题词:Carrier Proteins/metabolism*/载体蛋白质类/代谢*

主题词:Cyclin D1/metabolism/细胞周期蛋白D1/代谢

主题词:Epithelial-Mesenchymal Transition*/上皮细胞-间充质细胞转换*

主题词:LIM Domain Proteins/metabolism*/LIM结构域蛋白/代谢*

主题词:Uterine Cervical Neoplasms/pathology*/宫颈肿瘤/病理学*

主题词:Wnt Signaling Pathway*/Wnt信号通路*

全文链接:请使用FMRS数据库下载该篇文章。

 

 

编号:5

题名:LncRNA terminal differentiation-induced ncRNA (TINCR) sponges miR-302 to upregulate cyclin D1 in cervical squamous cell carcinoma (CSCC).

LncRNA末端分化诱导的ncRNATINCR)使miR-302上调宫颈鳞状细胞癌(CSCC)中的细胞周期蛋白D1

作者:Hou, A;Zhang, Y;Zheng, Y;Fan, Y;Liu, H;Zhou, X

出处:Hum Cell.2019,32(4):515-521

IF3.463

摘要:  This study aimed to investigate the role of lncRNA terminal differentiation-induced ncRNA (TINCR) in cervical squamous cell carcinoma (CSCC). By informatics analysis, we found that miR-302 may bind TINCR. Expression analysis showed that miR-302 was downregulated, while TINCR was upregulated in CSCC. Correlation analysis showed that they were not significantly correlated. In CSCC cells, miR-302 and TINCR failed to affect the expression of each other. However, miR-302 overexpression led to downregulated and TINCR overexpression led to upregulated cyclin D1 expression in CSCC cells. Interestingly, overexpression of cyclin D1 led to upregulated miR-302 and TINCR. Cell proliferation analysis showed that TINCR and cyclin D1 overexpression led to increased, while miR-302 overexpression led to decreased rate of cell proliferation. Moreover, miR-302 overexpression reduced the effects of TINCR overexpression. Therefore, TINCR sponges miR-302 to upregulate cyclin D1 in CSCC, thereby promoting cell proliferation.

主题词:Carcinoma, Squamous Cell/genetics*/, 鳞状细胞/遗传学*

主题词:Cyclin D1/genetics*/细胞周期蛋白D1/遗传学*

主题词:MicroRNAs/metabolism*/RNAs/代谢*

主题词:RNA, Long Noncoding/physiology*/RNA, 长链非编码/生理学*

主题词:Up-Regulation/genetics*/增量调节/遗传学*

主题词:Uterine Cervical Neoplasms/genetics*/宫颈肿瘤/遗传学*

全文链接:请使用FMRS数据库下载该篇文章。

 

 

编号:6

题名:≤Cyclin D1 protein affecting global women's health by regulating HPV mediated adenocarcinoma of the uterine cervix.

Cyclin D1蛋白通过调节HPV介导的子宫颈腺癌影响全球女性健康

作者:Tripathi, R;Rath, G;Jawanjal, P;Bharadwaj, M;Mehrotra, R

出处:Sci Rep.2019,9(1):5019

IF3.998

摘要:  Adenocarcinoma (ADC) of the uterine cervix (UC) is a rare form of cervical cancer (CC) caused due to the infection of Human Papilloma Virus (HPV). Cyclin D1 is one of the downstream targets of aberrantly activated Notch signaling, contribute to the etiology of CC. However, little is known about the role of Cyclin D1 in the modulation of cervical ADC and is controversial. The purpose of this study is to determine the role of Cyclin D1 protein and to elucidate the combined analysis with Notch signaling proteins in HPV associated ADCs of CC. A total of 60 biopsy samples (40 normal and 20 ADCs of CC) were analyzed for the expression of Cyclin D1 in HPV associated ADCs via immunohistochemistry and by immunoblotting. HPV-16 positive ADC patients showed a strong association with the Cyclin D1 expression (p=0.007). The significant mean difference (p=0.0001) and the pairwise comparison between Cyclin D1/JAG1 (p=0.0001), and Cyclin D1/Notch-3 (p=0.0001) were observed. The above Notch signaling proteins showed their synergistic role in modulating Cyclin D1 which in-turn regulates HPV-16 associated ADC of the uterine cervix (UC), affecting women's global health.

主题词:Adenocarcinoma/metabolism*/腺癌/代谢*

主题词:Cyclin D1/biosynthesis*/细胞周期蛋白D1/生物合成*

主题词:Human papillomavirus 16/isolation & purification*/人乳头瘤病毒16/分离与提纯*

主题词:Papillomavirus Infections/metabolism*/乳头状瘤病毒感染/代谢*

主题词:Uterine Cervical Neoplasms/metabolism*/宫颈肿瘤/代谢*

全文链接:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6430791/

 

 

编号:7

题名:Protein Dynamics in Complex DNA Lesions.

复杂DNA病变中的蛋白质动力学

作者:Aleksandrov, R;Dotchev, A;Poser, I;Krastev, D;Georgiev, G;Panova, G;Babukov, Y;Danovski, G;Dyankova, T;Hubatsch, L;Ivanova, A;Atemin, A;Nedelcheva-Veleva, MN;Hasse, S;Sarov, M;Buchholz, F;Hyman, AA;Grill, SW;Stoynov, SS

出处:Mol Cell.2018,69(6):1046-1061.e5

IF14.548

摘要:  A single mutagen can generate multiple different types of DNA lesions. How different repair pathways cooperate in complex DNA lesions, however, remains largely unclear. Here we measured, clustered, and modeled the kinetics of recruitment and dissociation of 70 DNA repair proteins to laser-induced DNA damage sites in HeLa cells. The precise timescale of protein recruitment reveals that error-prone translesion polymerases are considerably delayed compared to error-free polymerases. We show that this is ensured by the delayed recruitment of RAD18 to double-strand break sites. The time benefit of error-free polymerases disappears when PARP inhibition significantly delays PCNA recruitment. Moreover, removal of PCNA from complex DNA damage sites correlates with RPA loading during 5'-DNA end resection. Our systematic study of the dynamics of DNA repair proteins in complex DNA lesions reveals the multifaceted coordination between the repair pathways and provides a kinetics-based resource to study genomic instability and anticancer drug impact.

主题词:DNA Breaks, Double-Stranded*/drug effects/DNA断裂,双链*/药物作用

主题词:DNA Repair*/drug effects/DNA修复*/药物作用

主题词:DNA-Binding Proteins/metabolism*/DNA结合蛋白质类/代谢*

主题词:Ubiquitin-Protein Ligases/metabolism/泛素蛋白连接酶类/代谢

主题词:Uterine Cervical Neoplasms/metabolism*/宫颈肿瘤/代谢*

全文链接:请使用FMRS数据库下载该篇文章。

 

 

编号:8

题名:Tumor-suppressor gene SOX1 is a methylation-specific expression gene in cervical adenocarcinoma.

肿瘤抑制基因SOX1是宫颈腺癌中甲基化特异性表达基因

作者:Yuan, M;Yao, L;Abulizi, G

出处:Medicine (Baltimore).2019,98(38):e17225

IF1.552

摘要:  The present study is to analyze the difference of gene methylation in early cervical adenocarcinoma and to find molecular markers for predicting the occurrence and development of cervical adenocarcinoma.A total of 15 cases of primary cervical adenocarcinoma and 10 cases of primary cervical squamous cell carcinoma at stages IB1 or IIA1 were included in the study. Infinium MethylationEPIC BeadChip (850K) was used to screen specifically expressed genes in cervical adenocarcinoma tissues. Bisulfite sequencing polymerase chain reaction (BSP) and quantitative real-time polymerase chain reaction (qRT-PCR) were used to verify the methylation levels in cervical adenocarcinoma, cervical squamous cell carcinoma, and normal cervical tissues.Sex determining region Y-box 1 (SOX1) and cyclin D1 (CCND1) genes participated in multiple signaling pathways, being the central nodes of gene regulatory networks. SOX1 gene, but not CCND1 gene, was a specifically methylated gene in cervical adenocarcinoma according to BSP. According to qRT-PCR, methylation level of SOX1 in cervical adenocarcinoma tissues is significantly different from that in cervical squamous cell carcinoma tissues or normal cervical tissues, and the methylation level of CCND1 in cervical adenocarcinoma tissues or cervical squamous cell carcinoma tissues is significantly different from that in normal cervical tissues.The present study demonstrates that tumor-suppressor gene SOX1 is a methylation-specific expression gene of cervical adenocarcinoma and is expected to become a specific molecular marker for the diagnosis of cervical adenocarcinoma. However, CCND1 gene was not proven to be a specific methylation expression gene in cervical adenocarcinoma in the present study.

主题词:Adenocarcinoma/genetics*/腺癌/遗传学*

主题词:Cyclin D1/genetics/细胞周期蛋白D1/遗传学

主题词:DNA Methylation/genetics*/DNA甲基化/遗传学*

主题词:SOXB1 Transcription Factors/genetics*/SOXB1转录因子/遗传学*

主题词:Uterine Cervical Neoplasms/genetics*/宫颈肿瘤/遗传学*

全文链接:请使用FMRS数据库下载该篇文章。

 

 

编号:9

题名:Long non-coding RNA TP73 antisense RNA 1 facilitates the proliferation and migration of cervical cancer cells via regulating microRNA-607/cyclin D2.

长非编码RNA TP73反义RNA 1通过调节microRNA-607 /细胞周期蛋白D2促进宫颈癌细胞的增殖和迁移

作者:Zhang, H;Xue, B;Wang, S;Li, X;Fan, T

出处:Mol Med Rep.2019,20(4):3371-3378

IF2.1

摘要:  The present study aimed to explore the effect of the long non-coding RNA TP73 antisense RNA 1 (TP73-AS1) on cervical cancer progression. Cervical cancer and adjacent tissues were collected from 56 patients and assessed. In addition, HeLa and CaSki cells were transfected with various plasmids, inhibitors and corresponding controls, and then Cell Counting Kit-8 and Transwell assays were used to detect the cell proliferation, migration and invasion abilities. Luciferase reporter gene assay was also performed in HeLa cells. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to investigate TP73-AS1, microRNA-607 (miR-607) and cyclin D2 (CCND2) gene expression, while CCND2 protein expression was determined by western blot analysis. The results revealed that the TP73-AS1 level was upregulated in cervical cancer tissues (P<0.05) and predicted a poor 5-year overall survival (P<0.05). HeLa and CaSki cells transfected with siTP73-AS1 exhibited reduced proliferation, migration and invasion abilities when compared with those in the siNC group (P<0.05). Furthermore, miR-607 was found to be negatively regulated by TP73-AS1, while CCND2 was negatively regulated by miR-607. HeLa and CaSki cells transfected with siTP73-AS1 exhibited lower CCND2 mRNA and protein expression levels compared with the siNC and siTP73-AS1 + miR-inhibitor groups (P<0.05). Compared with the siNC and siTP73-AS1 + CCND2 overexpression groups, siTP73-AS1-transfected HeLa and CaSki cells had decreased proliferation, migration and invasion abilities (P<0.05). In conclusion, the findings suggested that upregulation of TP73-AS1 promoted cervical cancer progression by promoting CCND2 via the suppression of miR-607 expression.

主题词:Cell Proliferation*/细胞增殖*

主题词:Cyclin D2/biosynthesis*/细胞周期蛋白D2/生物合成*

主题词:Gene Expression Regulation, Neoplastic*/基因表达调控, 肿瘤*

主题词:MicroRNAs/biosynthesis*/RNAs/生物合成*

主题词:Neoplasm Proteins/biosynthesis*/肿瘤蛋白质类/生物合成*

主题词:RNA, Long Noncoding/metabolism*/RNA, 长链非编码/代谢*

主题词:RNA, Neoplasm/metabolism*/RNA, 肿瘤/代谢*

主题词:Uterine Cervical Neoplasms/metabolism*/宫颈肿瘤/代谢*

 

 

编号:10

题名:Motor Neuron and Pancreas Homeobox 1 (MNX1) Is Involved in Promoting Squamous Cervical Cancer Proliferation via Regulating Cyclin E.

运动神经元和胰腺同源框1MNX1)通过调节细胞周期蛋白E参与促进鳞状细胞癌的增殖

作者:Xiao, L;Hong, L;Zheng, W

出处:Med Sci Monit.2019,25:6304-6312

IF1.918

摘要:  BACKGROUND Cervical cancer is one of the most lethal gynecologic malignancies worldwide. The objective of this study was to assess the role of MNX1 in cervical cancer and its underlying mechanisms. MATERIAL AND METHODS The expression of motor neuron and pancreas homeobox 1 (MNX1) in immortal epithelial cervical cell line ECT, cervical cancer cell HeLa, and SiHa and cervical cancer, as well as in adjacent noncancer tissues, was detected and analyzed. CCK-8 and colony formation assays were performed to evaluate the effects of MNX1 overexpression on cervical cancer cell proliferation. Transwell assay was used to detect migration and invasion after MNX1 knockdown or overexpression. Real-time PCR and Western blotting were used to examine MNX1 and cell cycle regulator expression. RESULTS Data from our study indicated that MNX1 was upregulated both in cervical cancer cell lines and cervical cancer tissues. The high levels of MNX1 are related to advanced stages and lymph nodes metastasis. The overexpression of MNX1 promoted cervical cancer cells proliferation, migration, and invasion. Moreover, MNX1 upregulated 2 critical cell cycle regulators, CCNE1 and CCNE2. CONCLUSIONS These findings reveal MNX1 as a novel oncogene of cervical cancer and indicate MNX1 is a promising therapeutic and prognostic biomarker.

主题词:Cyclin E/genetics*/细胞周期蛋白E/遗传学*

主题词:Cyclins/genetics*/细胞周期蛋白类/遗传学*

主题词:Homeodomain Proteins/genetics*/同源盒结构域蛋白质类/遗传学*

主题词:Neoplasms, Squamous Cell/genetics*/肿瘤, 鳞状细胞/遗传学*

主题词:Oncogene Proteins/genetics*/癌基因蛋白质类/遗传学*

主题词:Transcription Factors/genetics*/转录因子/遗传学*

主题词:Uterine Cervical Neoplasms/genetics*/宫颈肿瘤/遗传学*

 

 

编号:11

题名:Targeting dipeptidyl peptidase 8 genes inhibits proliferation, migration and invasion by inhibition of cyclin D1 and MMP2MMP9 signal pathway in cervical cancer.

靶向二肽基肽酶8基因可通过抑制cyclin D1MMP2MMP9信号通路抑制宫颈癌的增殖,迁移和侵袭

作者:Chen, Y;Liu, F;Wu, K;Wu, W;Wu, H;Zhang, W

出处:J Gene Med.2018,20(12):e3056

IF1.561

摘要:  BACKGROUND:DPP8 is a member of the dipeptidyl peptidase IV family, which belongs to the S9b protease subfamily. It regulates cell proliferation, apoptosis, migration and invasion during cancer progression. METHODS:To investigate the role of DPP8 in cervical cancer, we examined DPP8 levels in cervical cancer tissues and cells. The localization of DPP8 was determined by immunofluorescence staining. Subsequently, SiHa and HeLa cells were treated with small interfering RNA (siRNA)-DPP8. We used cell cycle analysis, an 5-ethyl-2'-deoxyuridine assay proliferation assay and a cellular apoptosis assay to determine the effect of DPP8 on the proliferation and apoptosis of cervical cancer cells. We used a Transwell assay to assess the number of transfection cancer cells migrating through the matrix. A real-time polymerase chain reaction and western blot analysis were used to analyze the expression of related proteins and to determine the phenotype caused by the depletion or overexpression of DPP8 in cervical cancer cells. RESULTS:We observed that DPP8 was highly expressed in cervical cancer tissues and cells. DPP8 expression was observed in the cytosol and in the perinuclear area, as well as in the nuclei of cervical cancer cells. Notably, when cells were treated with siRNA-DPP8, the expression of BAX increased, and the expression of cyclin D1, Bcl-2, MMP2 and MMP9 was downregulated. In cervical cancer cell lines, silencing the expression of DPP8 not only suppressed the proliferation, migration and invasion of the cervical cancer cells, but also promoted cervical cancer cell apoptosis. CONCLUSIONS:The data obtained in the present study reveal that DPP8 promotes the progression of cervical cancer.

主题词:Cell Movement/genetics*/细胞运动/遗传学*

主题词:Cell Proliferation/genetics*/细胞增殖/遗传学*

主题词:Cyclin D1/metabolism/细胞周期蛋白D1/代谢

主题词:Dipeptidases/genetics*/二肽酶类/遗传学*

主题词:RNA Interference*/RNA干扰*

主题词:Signal Transduction/genetics*/信号传导/遗传学*

主题词:Uterine Cervical Neoplasms/genetics*/宫颈肿瘤/遗传学*

全文链接:请使用FMRS数据库下载该篇文章。

 

 

编号:12

题名:HMGA1 exacerbates tumor growth through regulating the cell cycle and accelerates migration/invasion via targeting miR-221/222 in cervical cancer.

HMGA1通过调节细胞周期加剧肿瘤的生长,并通过靶向miR-221 / 222加速子宫颈癌的迁移/侵袭

作者:Fu, F;Wang, T;Wu, Z;Feng, Y;Wang, W;Zhou, S;Ma, X;Wang, S

出处:Cell Death Dis.2018,9(6):594

IF5.959

摘要:  High-mobility group AT-hook1 (HMGA1, formerly HMG-I/Y), an architectural transcription factor, participates in a number of tumor biological processes. However, its effect on cervical cancer remains largely indistinct. In this study, we found that HMGA1 was generally overexpressed in cervical cancer tissues and was positively correlated with lymph node metastasis and advanced clinical stage. Via exogenously increasing or decreasing the expression of HMGA1, we showed that HMGA1 affected the proliferation, colony formation, migration and invasion of cervical cancer cells in vitro. Rescue experiments suggested that miR-221/222 could partly reverse HMGA1-mediated migration and invasion processes. Mechanistically, we discovered that HMGA1 accelerated the G1/S phase transition by regulating the expression of cyclin D1 and cyclin E1, which was consistent with the results of the in vivo experiment. Furthermore, we found that HMGA1 regulated the expression of the miR-221/222 cluster at the transcriptional level and that miR-221/222 targeted the 3'UTR of tissue inhibitor of metalloproteinases 3(TIMP3). We propose a fresh perspective that HMGA1 participates in the migration and invasion process via the miR-221/222-TIMP3-MMP2/MMP9 axis in cervical cancer. In summary, our study identified a critical role played by HMGA1 in the progression of cervical cancer and the potential mechanisms by which exerts its effects, suggesting that targeting HMGA1-related pathways could be conducive to the therapies for cervical cancer.

主题词:Cell Cycle/genetics*/细胞周期/遗传学*

主题词:Cell Movement/genetics*/细胞运动/遗传学*

主题词:Cyclin D1/metabolism/细胞周期蛋白D1/代谢

主题词:Cyclin E/metabolism/细胞周期蛋白E/代谢

主题词:G1 Phase/genetics/G1/遗传学

主题词:HMGA1a Protein/metabolism*/HMGA1a蛋白/代谢*

主题词:MicroRNAs/metabolism*/RNAs/代谢*

主题词:Uterine Cervical Neoplasms/genetics*/宫颈肿瘤/遗传学*

主题词:Uterine Cervical Neoplasms/pathology*/宫颈肿瘤/病理学*

全文链接:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5964147/

 

 

编号:13

题名:Baicalein blocked cervical carcinoma cell proliferation by targeting CCND1 via Wnt/β-catenin signaling pathway.

黄芩素通过Wnt /β-连环蛋白信号通路靶向CCND1阻断宫颈癌细胞增殖

作者:Xia, X;Xia, J;Yang, H;Li, Y;Liu, S;Cao, Y;Tang, L;Yu, X

出处:Artif Cells Nanomed Biotechnol.2019,47(1):2729-2736

IF3.343

摘要:  The purpose of this study was to investigate the inhibitory effect of baicalein on the proliferation of cervical carcinoma cells and stimulate cervical carcinoma cells with baicalein. MTT method was used to observe cell proliferation. Flow cytometry was used to observe cell cycle, and gene technology was used to observe the expression of corresponding genes at the level of gene and protein. β-catenin activity was assessed using Western blot and ChIP. Baicalein suppressed cervical carcinoma cell HeLa proliferation by enhancing the activity of caspase-3. Baicalein blocked cell cycle at G0/G1 stage by inhibiting the expression of some genes. At the same time, it can prevent the nuclear translocation of β-catenin and inhibit the activity of Wnt. When the Wnt signaling pathway is increased, the proliferation of HeLa cells is inhibited, and apoptosis is promoted in this way. In conclusion, it indicated that baicalein inhibits cervical carcinoma progression by targeting CCND1 via Wnt/β-catenin signaling pathway.

主题词:Antineoplastic Agents/pharmacology*/抗肿瘤药/药理学*

主题词:Cyclin D1/metabolism*/细胞周期蛋白D1/代谢*

主题词:Flavanones/pharmacology*/黄烷酮类/药理学*

主题词:Molecular Targeted Therapy*/分子靶向治疗*

主题词:Uterine Cervical Neoplasms/pathology*/宫颈肿瘤/病理学*

主题词:Wnt Signaling Pathway/drug effects*/Wnt信号通路/药物作用*

全文链接:请使用FMRS数据库下载该篇文章。

 

 

编号:14

题名:Metformin Modulates Cyclin D1 and P53 Expression to Inhibit Cell Proliferation and to Induce Apoptosis in Cervical Cancer Cell Lines.

二甲双胍调节细胞周期蛋白D1P53的表达,抑制细胞增殖,诱导宫颈癌细胞凋亡

作者:Yudhani, RD;Astuti, I;Mustofa, M;Indarto, D;Muthmainah, M

出处:Asian Pac J Cancer Prev.2019,20(6):1667-1673

摘要:  Background: Cervical cancer is one of the most prevalent gynecological cancers worldwide and contributes in high mortality of Indonesian women. The efficacy of chemotherapy as a standart therapy for cervical cancer decreases because it frequenly rises adverse effects. Recent studies have found that metformin has a potential anticancer effect mostly through reduction of cyclin expression and activation of Activated Adenosine Monophosphate Kinase (AMPK). This study aimed to investigate the effect of metfomin on expression of cyclin D1 and p53 and apoptosis in HeLa cancer cell line. Methods: HeLa cells were treated with various doses of metformin and doxorubicin as a positive control. Cytotoxic effect of metformin was determined using the MTT assay. Immunocytochemistry was used to assess cyclin D1 and p53 expression and apoptosis levels of treated HeLa cells were analyzed using flowcytometry. Data of cyclin D1 expression was statistically analyzed using the Kruskal-Wallis test followed by the Tamhane test, whilst ANOVA and Tukey post Hoc tests were used to analyze data of p53 and apoptosis level. The significant value was p< 0.05. Results: Metformin was able to inhibit proliferation of HeLa cells with IC50 60 mM. HeLa cells treated with 60 and 120 mM metformin had lower cyclin D1 expression than HeLa cells treated without metformin and reached a significant difference (p= 0.001). Moreover, 30 mM or higher doses of metformin increase significantly p53 expression (p< 0.001). Induction of apoptosis was observed in HeLa cells treated with all doses of metformin and reached statistically difference (p= 0.04 and p < 0.001). Conclusion: Metformin can modulate cyclin D1 and p53 expression in HeLa cancer cell line, leading to inhibition of cell proliferation and induction of apoptosis. Other cyclin family members, CDK inhibitors and AMPK signaling should be further investigated in order to know mechanism of metformin action.

主题词:Apoptosis/drug effects*/细胞凋亡/药物作用*

主题词:Cell Proliferation/drug effects*/细胞增殖/药物作用*

主题词:Cyclin D1/metabolism*/细胞周期蛋白D1/代谢*

主题词:Hypoglycemic Agents/pharmacology*/降血糖药/药理学*

主题词:Metformin/pharmacology*/二甲双胍/药理学*

主题词:Tumor Suppressor Protein p53/metabolism*/肿瘤抑制蛋白质p53/代谢*

主题词:Uterine Cervical Neoplasms/pathology*/宫颈肿瘤/病理学*

全文链接:

http://journal.waocp.org/article_88248_82720f9e76a77c2f600a0c134d80044c.pdf

 

 

编号:15

题名:PDZ Domain-Containing Protein NHERF-2 Is a Novel Target of Human Papillomavirus 16 (HPV-16) and HPV-18.

PDZ域包含蛋白NHERF-2是人类乳头瘤病毒16HPV-16)和HPV-18的新型靶标

作者:Saidu, NEB;Fili?, V;Thomas, M;Sarabia-Vega, V;?uki?, A;Miljkovi?, F;Banks, L;Tomai?, V

出处:J Virol.2019,94(1):

IF4.501

摘要:  Cancer-causing human papillomavirus (HPV) E6 oncoproteins have a class I PDZ-binding motif (PBM) on their C termini, which play critical roles that are related to the HPV life cycle and HPV-induced malignancies. E6 oncoproteins use these PBMs to interact with, to target for proteasome-mediated degradation, a plethora of cellular substrates that contain PDZ domains and that are involved in the regulation of various cellular pathways. In this study, we show that both HPV-16 and HPV-18 E6 oncoproteins can interact with Na+/H+ exchange regulatory factor 2 (NHERF-2), a PDZ domain-containing protein, which among other cellular functions also behaves as a tumor suppressor regulating endothelial proliferation. The interaction between the E6 oncoproteins and NHERF-2 is PBM dependent and results in proteasome-mediated degradation of NHERF-2. We further confirmed this effect in cells derived from HPV-16- and HPV-18-positive cervical tumors, where we show that NHERF-2 protein turnover is increased in the presence of E6. Finally, our data indicate that E6-mediated NHERF-2 degradation results in p27 downregulation and cyclin D1 upregulation, leading to accelerated cellular proliferation. To our knowledge, this is the first report to demonstrate that E6 oncoproteins can stimulate cell proliferation by indirectly regulating p27 through targeting a PDZ domain-containing protein.IMPORTANCE This study links HPV-16 and HPV-18 E6 oncoproteins to the modulation of cellular proliferation. The PDZ domain-containing protein NHERF-2 is a tumor suppressor that has been shown to regulate endothelial proliferation; here, we demonstrate that NHERF-2 is targeted by HPV E6 for proteasome-mediated degradation. Interestingly, this indirectly affects p27, cyclin D1, and CDK4 protein levels and, consequently, affects cell proliferation. Hence, this study provides information that will improve our understanding of the molecular basis for HPV E6 function, and it also highlights the importance of the PDZ domain-containing protein NHERF-2 and its tumor-suppressive role in regulating cell proliferation.

主题词:Cyclin D1/metabolism/细胞周期蛋白D1/代谢

主题词:DNA-Binding Proteins/genetics*/DNA结合蛋白质类/遗传学*

主题词:Host-Pathogen Interactions/genetics*/宿主-病原体相互作用/遗传学*

主题词:Human papillomavirus 16/genetics*/人乳头瘤病毒16/遗传学*

主题词:Human papillomavirus 18/genetics*/人乳头瘤病毒18/遗传学*

主题词:Oncogene Proteins, Viral/genetics*/癌基因蛋白质类, 病毒性/遗传学*

主题词:Phosphoproteins/genetics*/磷蛋白类/遗传学*

主题词:Repressor Proteins/genetics*/阻遏蛋白质类/遗传学*

主题词:Sodium-Hydrogen Exchangers/genetics*/钠氢交换器/遗传学*

主题词:Uterine Cervical Neoplasms/metabolism/宫颈肿瘤/代谢

全文链接:请使用FMRS数据库下载该篇文章。

 

 

编号:16

题名:Regulatory mechanisms of fluvastatin and lovastatin for the p21 induction in human cervical cancer HeLa cells.

氟伐他汀和洛伐他汀在人宫颈癌HeLa细胞中诱导p21的调控机制

作者:Lin, CK;Liu, ST;Chang, CC;Huang, SM

出处:PLoS One.2019,14(4):e0214408

IF2.74

摘要:  p21, an inhibitor of cyclin-dependent kinase, functions as an oncogene or tumor suppressor depending on the context of a variety of extracellular and intracellular signals. The expression of p21 could be regulated at the transcriptional and/or post-translational levels. The p21 gene is well-known to be regulated in both p53-dependent and -independent manners. However, the detailed regulatory mechanisms of p21 messenger RNA and protein expression via statins remain unknown, and the possible application of statins as anticancer reagents remains to be controversial. Our data showed that the statins-fluvastatin and lovastatin-induced p21 expression as general histone deacetylase inhibitors in a p53-independent manner, which is mediated through various pathways, such as apoptosis, autophagy, cell cycle progression, and DNA damage, to be involved in the function of p21 in HeLa cells. The curative effect repositioning of digoxin, a cardiovascular medication, was combined with fluvastatin and lovastatin, and the results further implied that p21 induction is involved in a p53-dependent and p53-independent manner. Digoxin modified the effects of statins on ATF3, p21, p53, and cyclin D1 expression, while fluvastatin boosted its DNA damage effect and lovastatin impeded its DNA damage effect. Fluvastatin and lovastatin combined with digoxin further support the localization specificity of their interactivity with our subcellular localization data. This study will not only clarify the regulatory mechanisms of p21 induction by statins but will also shed light on the repurposing of widely cardiovascular medications for the treatment of cervical cancer.

主题词:Cyclin D1/genetics/细胞周期蛋白D1/遗传学

主题词:Cyclin-Dependent Kinase Inhibitor p21/genetics*/周期素依赖激酶抑制剂p21/遗传学*

主题词:Lovastatin/pharmacology*/洛伐他汀/药理学*

主题词:Uterine Cervical Neoplasms/drug therapy*/宫颈肿瘤/药物疗法*

全文链接:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6445431/

 

 

编号:17

题名:The long non-coding RNA PTTG3P promotes growth and metastasis of cervical cancer through PTTG1.

长非编码RNA PTTG3P通过PTTG1促进宫颈癌的生长和转移

作者:Guo, XC;Li, L;Gao, ZH;Zhou, HW;Li, J;Wang, QQ

出处:Aging (Albany NY).2019,11(5):1333-1341

IF4.831

摘要:  The outgrowth and metastasis of cervical cancer (CC) contribute to its malignancy. Pituitary Tumor Transforming Gene 1 (PTTG1) is upregulated in many types of cancer, and enhances tumor cell growth and metastasis. However, the activation and regulation of PTTG1 in CC, especially by its pseudogene PTTG3P, have not been shown. Here, we detected significantly higher levels of PTTG1 and PTTG3P in the resected CC tissue, compared to the paired adjacent normal cervical tissue. Interestingly, the PTTG3P levels positively correlated with the PTTG1 levels. High PTTG3P levels were associated with poor patients' survival. In vitro, PTTG1 were increased by PTTG3P overexpression, but was inhibited by PTTG3P depletion in CC cells. However, PTTG3P levels were not altered by modulation of PTTG1 in CC cells, suggesting that PTTG3P is upstream of PTTG1. Moreover, PTTG3P increased CC cell growth, likely through CCNB1-mediated increase in cell proliferation, rather than through decrease in cell apoptosis. Furthermore, PTTG3P increased CC cell invasiveness, likely through upregulation of SNAIL and downregulation of E-cadherin. Our work thus suggests that PTTG3P may promote growth and metastasis of CC through PTTG1.

主题词:Cyclin B1/metabolism/细胞周期蛋白B1/代谢

主题词:RNA, Long Noncoding/metabolism*/RNA, 长链非编码/代谢*

主题词:Securin/metabolism*/分离酶抑制蛋白/代谢*

主题词:Uterine Cervical Neoplasms/metabolism*/宫颈肿瘤/代谢*

主题词:Uterine Cervical Neoplasms/pathology*/宫颈肿瘤/病理学*

全文链接:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6428096/

 

 

编号:18

题名:A novel biphenyl urea compound, TPD7, stimulates apoptosis through modulating Fas signaling and Bcl-2 family proteins in cervical cancer.

新型联苯脲化合物TPD7通过调节Fas信号传导和Bcl-2家族蛋白刺激宫颈癌细胞凋亡

作者:Zhan, Y;Zhang, H;Dai, B;Zhang, Y;Zhang, J;He, L

出处:Oncol Rep.2018,40(2):1064-1072

IF3.041

摘要:  We recently reported that TPD7 suppressed tumor cell proliferation, and inhibited invasion, through the suppression of C-X-C chemokine receptor type 4 (CXCR4). In the present study, we investigated the anticancer effect of TPD7 on apoptosis and invasion of cervical cancer HeLa cells. Cell cycle analysis revealed that TPD7 decreased cyclin-dependent kinase (CDK)1 and cyclin D1 expression, and increased cyclin A expression, following S phase blockade. TPD7 induced chromatin condensation and significantly elevated the number of apoptotic cells, suggesting that its inhibitory effect on HeLa cells was due to the induction of cell cycle blockade and apoptosis. Mechanistically, TPD7 altered the extrinsic apoptosis pathway by upregulating Fas expression, and the intrinsic pathway by modulating Bcl-2 family proteins, p53, and NF-κB p65, leading to enhanced apoptosis. TPD7 inhibited HeLa cell invasion by downregulating the expression of matrix metalloproteinase (MMP)-9 and CXCR4 proteins. In vivo experiments revealed that TPD7 inhibited tumor growth in HeLa cell xenografted mice. These findings indicated that TPD7 may be a potential chemoprevention agent for the management of cervical carcinoma.

主题词:Apoptosis/drug effects*/细胞凋亡/药物作用*

主题词:Biphenyl Compounds/pharmacology*/联苯化合物/药理学*

主题词:Carbanilides/pharmacology*/二苯脲类/药理学*

主题词:Cyclin D1/metabolism/细胞周期蛋白D1/代谢

主题词:Hydroxylamines/pharmacology*/羟胺类/药理学*

主题词:Matrix Metalloproteinase 9/metabolism/基质金属蛋白酶9/代谢

主题词:Proto-Oncogene Proteins c-bcl-2/metabolism*/原癌基因蛋白质c-bcl-2/代谢*

主题词:Uterine Cervical Neoplasms/drug therapy*/宫颈肿瘤/药物疗法*

主题词:fas Receptor/metabolism*/fas受体/代谢*

全文链接:请使用FMRS数据库下载该篇文章。

 

 

编号:19

题名:SNAP23 suppresses cervical cancer progression via modulating the cell cycle.

SNAP23通过调节细胞周期来抑制宫颈癌的进展

作者:Zhu, B;Zhang, Q;Wu, Y;Luo, J;Zheng, X;Xu, L;Lu, E;Qu, J;Ren, B

出处:Gene.2018,673:217-224

IF2.638

摘要:  OBJECTIVE:Cervical cancer (CC) is one of the most common gynecologic tumors in women worldwide, with poor prognosis and low survival rate. In this study, we identified SNAP23 as a potential tumor suppressor gene in CC. METHODS:The expression of SNAP23 in tissues and cell lines were measured by qRT-PCR, western blot and IHC. Knockdown of SNAP23 by siRNA and ectopic expression of SNAP23 by overexpression plasmid were performed to observe the biological function of SNAP23 in CC. Xenograft nude mice models were established to measure its function in vivo. RESULTS:SNAP23 was downregulated in CC tissues and had a negative correlation with advanced clinical characteristics. Ectopic expression of SNAP23 suppressed malignant phonotype of CC while knockdown of SNAP23 promoted the progression of CC in vitro. The flow cytometry analysis revealed that SNAP23 exerted its tumor suppressor activity via inducing G2/M cell cycle arrest. Moreover, xenograft tumor models showed that SNAP23 suppresses tumor growth in vivo. CONCLUSIONS:Our results revealed that SNAP23 suppressed progression of CC and induced cell cycle G2/M arrest via upregulating p21cip1 and downregulating CyclinB1.

主题词:Cell Cycle*/细胞周期*

主题词:Cyclin B1/metabolism*/细胞周期蛋白B1/代谢*

主题词:Cyclin-Dependent Kinase Inhibitor p21/metabolism*/周期素依赖激酶抑制剂p21/代谢*

主题词:Qb-SNARE Proteins/genetics*/Qb-SNARE蛋白质类/遗传学*

主题词:Qb-SNARE Proteins/metabolism/Qb-SNARE蛋白质类/代谢

主题词:Qc-SNARE Proteins/genetics*/Qc-SNARE蛋白质类/遗传学*

主题词:Uterine Cervical Neoplasms/genetics*/宫颈肿瘤/遗传学*

全文链接:请使用FMRS数据库下载该篇文章。

 

 

编号:20

题名:Combination of RIZ1 Overexpression and Radiotherapy Contributes to Apoptosis and DNA Damage of HeLa and SiHa Cervical Cancer Cells.

RIZ1过表达与放射治疗相结合有助于HeLaSiHa宫颈癌细胞的凋亡和DNA损伤

作者:Yang, S;Xing, L;Gu, L;Cheng, H;Feng, Y;Zhang, Y

出处:Basic Clin Pharmacol Toxicol.2018,123(2):137-146

IF2.452

摘要:  Although radiotherapy has been widely applied to treating cervical cancer in the clinic, its therapeutic efficacy is often restricted to the radioresistance of cancer cells. Retinoblastoma protein-interacting zinc finger gene 1 (RIZ1) has been suggested as a tumour suppressor gene, whereas its role in cervical cancer with or without radiotherapy has been unclear. In this study, two cervical cancer cell lines, HeLa and SiHa cells, stably transfected with RIZ1 overexpression plasmid were subjected to ionizing radiation, and their survival fractions were calculated by assessing their clonogenic abilities. Our results showed that the forced overexpression of RIZ1 significantly reduced the clonogenic survival rates of both HeLa and SiHa cells exposed to ionizing radiation. By analysing the cell apoptotic status, we found that the RIZ1-overexpressed cervical cancer cells under ionizing radiation were more vulnerable to damage, and more γ-H2AX foci were found in these cells. Furthermore, the volumes of tumour xenografts formed by the RIZ1-overexpressed cells in nude mice under ionizing radiation were smaller than those generated by the control cells. There were more morphological changes, apoptosis cells and lower expression of PCNA in RIZ1-overexpressed tumour tissues of mice after exposure to ionizing radiation. Taken together, our study demonstrates that the overexpression of RIZ1 combined with radiotherapy facilitates apoptosis and DNA damage of cervical cancer cells.

主题词:DNA Damage/radiation effects*/DNA损伤/辐射效应*

主题词:DNA-Binding Proteins/metabolism*/DNA结合蛋白质类/代谢*

主题词:Genes, Tumor Suppressor*/基因, 肿瘤抑制*

主题词:Histone-Lysine N-Methyltransferase/metabolism*/组蛋白赖氨酸N-甲基转移酶/代谢*

主题词:Nuclear Proteins/metabolism*/核蛋白质类/代谢*

主题词:Transcription Factors/metabolism*/转录因子/代谢*

主题词:Uterine Cervical Neoplasms/therapy*/宫颈肿瘤/治疗*

全文链接:请使用FMRS数据库下载该篇文章。

 

 

编号:21

题名:CircRNA8924 Promotes Cervical Cancer Cell Proliferation, Migration and Invasion by Competitively Binding to MiR-518d-5p /519-5p Family and Modulating the Expression of CBX8.

CircRNA8924通过竞争性结合MiR-518d-5p / 519-5p家族并调节CBX8的表达促进宫颈癌细胞增殖,迁移和侵袭

作者:Liu, J;Wang, D;Long, Z;Liu, J;Li, W

出处:Cell Physiol Biochem.2018,48(1):173-184

主题词:Cyclin D1/metabolism/细胞周期蛋白D1/代谢

主题词:G1 Phase Cell Cycle Checkpoints/G1期细胞周期检查点

主题词:MicroRNAs/metabolism*/RNAs/代谢*

主题词:Polycomb Repressive Complex 1/metabolism*/多梳抑制复合体1/代谢*

主题词:RNA/metabolism*/RNA/代谢*

主题词:Uterine Cervical Neoplasms/pathology*/宫颈肿瘤/病理学*

全文链接:请使用FMRS数据库下载该篇文章。

 

 

编号:22

题名:Expression of the cervical carcinoma expressed PCNA regulatory (CCEPR) long noncoding RNA is driven by the human papillomavirus E6 protein and modulates cell proliferation independent of PCNA.

宫颈癌表达的PCNA调节(CCEPR)长非编码RNA由人乳头瘤病毒E6蛋白驱动并调节细胞增殖而不依赖于PCNA

作者:Sharma, S;Munger, K

出处:Virology.2018,518:8-13

IF2.657

摘要:  Modulation of expression of noncoding RNAs is an important aspect of the oncogenic activities of high-risk human papillomavirus (HPV) E6 and E7 proteins. While HPV E6/E7-mediated alterations of microRNAs (miRNAs) has been studied in detail there are fewer reports on HPV-mediated dysregulation of long noncoding RNAs (lncRNAs). The cervical carcinoma expressed PCNA regulatory (CCEPR) lncRNA is highly expressed in cervical cancers and expression correlates with tumor size and patient outcome. We report that CCEPR is a nuclear lncRNA and that HPV16 E6 oncogene expression causes increased CCEPR expression through a mechanism that is not directly dependent on TP53 inactivation. CCEPR depletion in cervical carcinoma cell lines reduces viability, while overexpression enhances viability. In contrast to what was published and inspired its designation, there is no evidence for PCNA mRNA stabilization, and hence CCEPR likely functions through a different mechanism.

主题词:Carcinoma/metabolism*//代谢*

主题词:Cell Proliferation/physiology*/细胞增殖/生理学*

主题词:Oncogene Proteins, Viral/metabolism*/癌基因蛋白质类, 病毒性/代谢*

主题词:Proliferating Cell Nuclear Antigen/metabolism*/增殖细胞核抗原/代谢*

主题词:RNA, Long Noncoding/metabolism*/RNA, 长链非编码/代谢*

主题词:Repressor Proteins/metabolism*/阻遏蛋白质类/代谢*

主题词:Uterine Cervical Neoplasms/metabolism*/宫颈肿瘤/代谢*

全文链接:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5911229

 

 

编号:23

题名:Blocking 17β-hydroxysteroid dehydrogenase type 1 in endometrial cancer: a potential novel endocrine therapeutic approach.

在子宫内膜癌中阻断117β-羟基类固醇脱氢酶:一种潜在的新型内分泌治疗方法

作者:Konings, GF;Cornel, KM;Xanthoulea, S;Delvoux, B;Skowron, MA;Kooreman, L;Koskimies, P;Krakstad, C;Salvesen, HB;van Kuijk, K;Schrooders, YJ;Vooijs, M;Groot, AJ;Bongers, MY;Kruitwagen, RF;ENITEC;Romano, A

出处:J Pathol.2018,244(2):203-214

IF5.942

摘要:  The enzyme type 1 17β-hydroxysteroid dehydrogenase (17β-HSD-1), responsible for generating active 17β-estradiol (E2) from low-active estrone (E1), is overexpressed in endometrial cancer (EC), thus implicating an increased intra-tissue generation of E2 in this estrogen-dependent condition. In this study, we explored the possibility of inhibiting 17β-HSD-1 and impairing the generation of E2 from E1 in EC using in vitro, in vivo, and ex vivo models. We generated EC cell lines derived from the well-differentiated endometrial adenocarcinoma Ishikawa cell line and expressing levels of 17β-HSD-1 similar to human tissues. In these cells, HPLC analysis showed that 17β-HSD-1 activity could be blocked by a specific 17β-HSD-1 inhibitor. In vitro, E1 administration elicited colony formation similar to E2, and this was impaired by 17β-HSD-1 inhibition. In vivo, tumors grafted on the chicken chorioallantoic membrane (CAM) demonstrated that E1 upregulated the expression of the estrogen responsive cyclin A similar to E2, which was impaired by 17β-HSD-1 inhibition. Neither in vitro nor in vivo effects of E1 were observed using 17β-HSD-1-negative cells (negative control). Using a patient cohort of 52 primary ECs, we demonstrated the presence of 17β-HSD-1 enzyme activity (ex vivo in tumor tissues, as measured by HPLC), which was inhibited by over 90% in more than 45% of ECs using the 17β-HSD-1 inhibitor. Since drug treatment is generally indicated for metastatic/recurrent and not primary tumor, we next demonstrated the mRNA expression of the potential drug target, 17β-HSD-1, in metastatic lesions using a second cohort of 37 EC patients. In conclusion, 17β-HSD-1 inhibition efficiently blocks the generation of E2 from E1 using various EC models. Further preclinical investigations and 17β-HSD-1 inhibitor development to make candidate compounds suitable for the first human studies are awaited. Copyright  2017 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

主题词:Antineoplastic Agents/pharmacology*/抗肿瘤药/药理学*

主题词:Cell Proliferation/drug effects*/细胞增殖/药物作用*

主题词:Cyclin A/metabolism/细胞周期蛋白A/代谢

主题词:Endometrial Neoplasms/drug therapy*/子宫内膜肿瘤/药物疗法*

主题词:Enzyme Inhibitors/pharmacology*/酶抑制剂/药理学*

主题词:Estradiol Dehydrogenases/antagonists & inhibitors*/雌二醇脱氢酶类/拮抗剂与抑制剂*

全文链接:请使用FMRS数据库下载该篇文章。

 

 

编号:24

题名:Identification of novel cyclin gene fusion transcripts in endometrioid ovarian carcinomas.

子宫内膜样卵巢癌新细胞周期蛋白基因融合转录本鉴定

作者:Agostini, A;Brunetti, M;Davidson, B;G?ran Tropé, C;Heim, S;Panagopoulos, I;Micci, F

出处:Int J Cancer.2018,143(6):1379-1387

IF4.982

摘要:  Formation of fusion genes is pathogenetically crucial in many solid tumors. They are particularly characteristic of several mesenchymal tumors, but may also be found in epithelial neoplasms. Ovarian carcinomas, too, may harbor fusion genes but only few of these were found to be recurrent with a rate ranging from 0.5 to 5%. Because most attempts to find specific and recurrent fusion transcripts in ovarian carcinomas focused exclusively on high-grade serous carcinomas, the situation in the other carcinoma subgroups remains largely uninvestigated as far as fusion genes are concerned. We performed transcriptome sequencing on a series of 34 samples from ovarian tumors that included borderline, clear cell, mucinous, endometrioid, low-grade and high-grade serous carcinomas in search of fusion genes typical of these subtypes. We found a total of 24 novel fusion transcripts. The PCMTDI-CCNL2 fusion transcript, which involves a member of the cyclin family, was found recurrently involved but only in endometrioid carcinomas (4 of 18 tumors; 22%). We also found three additional fusion transcripts involving genes belonging to the cyclin family: ANXA5-CCNA2 and PDE4D-CCNB1 were detected in two endometrioid carcinomas, whereas CCNY-NRG4 was identified in a clear cell carcinoma. The recurrent involvement of CCNL2 in four fusions and of three other genes of the cyclin family in three additional transcripts hints that deregulation of cyclin genes is important in the pathogenesis of ovarian carcinomas in general but of endometrioid carcinomas particularly.

主题词:Cyclins/genetics*/细胞周期蛋白类/遗传学*

主题词:Endometrial Neoplasms/genetics*/子宫内膜肿瘤/遗传学*

主题词:Gene Fusion*/基因融合*

主题词:Neoplasm Recurrence, Local/genetics*/肿瘤复发, 局部/遗传学*

主题词:Oncogene Proteins, Fusion/genetics*/癌基因蛋白质类, 融合/遗传学*

主题词:Ovarian Neoplasms/genetics*/卵巢肿瘤/遗传学*

全文链接:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6099316/

 

 

编号:25

题名:Synergistic effect of metformin and medroxyprogesterone 17-acetate on the development of endometrial cancer.

二甲双胍和17-乙酸甲羟孕酮对子宫内膜癌发展的协同作用

作者:Mu, N;Dong, M;Li, L;Xia, M;Qv, L;Wang, Y;Dong, C;Chen, Y;Zuo, Y;Hou, J;Xue, F

出处:Oncol Rep.2018,39(4) :2015-2021

IF3.041

摘要:  Accumulating data indicate that insulin resistance and unopposed estrogen are important risk factors of endometrial cancer (EC). Medroxyprogesterone 17-acetate (MPA) has been used in the treatment of EC for many years. However, the therapeutic effect of this agent on EC has not been satisfactory. 36 arMetformin was recently reported to be a promising agent for the treatment of malignant diseases including EC. However, information on the synergistic effect of the two agents in EC is limited. With the aim to evaluate the synergistic effect of metformin and MPA, we conducted the present study in?vitro and in?vivo. We found that the combined application of metformin and MPA significantly inhibited the proliferation of the Ishikawa cells and arrested the cells in the G0/G1 phase. Furthermore, the apoptosis rate of the Ishikawa cells was significantly increased. In the animal study, the development of the xenograft tumors was significantly suppressed by the combined application of the two agents. Further investigation revealed that the synergistic inhibitory effect of the two agents on EC can be at least partly, explained by the decreased expression of cyclin D1 and cyclin E. The results of the current study provide novel insights into the treatment of EC.

主题词:Cell Cycle Checkpoints/drug effects/细胞周期检查点/药物作用

主题词:Cyclin D1/genetics/细胞周期蛋白D1/遗传学

主题词:Cyclin E/genetics/细胞周期蛋白E/遗传学

主题词:Drug Synergism*/药物协同作用*

主题词:Endometrial Neoplasms/drug therapy*/子宫内膜肿瘤/药物疗法*

主题词:Medroxyprogesterone Acetate/pharmacology*/醋酸甲羟孕酮/药理学*

主题词:Metformin/pharmacology*/二甲双胍/药理学*

全文链接:请使用FMRS数据库下载该篇文章。

 

 

编号:26

题名:miR-142 Suppresses Endometrial Cancer Proliferation In Vitro and In Vivo by Targeting Cyclin D1.

miR-142通过靶向Cyclin D1抑制体外和体内子宫内膜癌的增殖

作者:Su, Y;Wang, J;Ma, Z;Gong, W;Yu, L

出处:DNA Cell Biol.2019,38(2):144-150

IF2.918

摘要:  Endometrial cancer (EC), a prevalent gynecologic tumor, is a great threat to women. We aimed to explore miR-142's effects on EC and the relevant mechanisms. Cell proliferation was evaluated with MTT, cell counting, and colony formation assay. MRNA abundances of miR-142 and cyclin D1 (CCND1) were examined with quantitative real-time PCR. CCND1 protein level in cells was analyzed with Western blot. miR-142's downstream target was identified with targetscan and luciferase reporter assay. Nude mice were injected subcutaneously with Ishikawa (ISK) cells transfected with or without miR-142 mimics. Ki-67 and CCND1 expressions in tumors of xenograft mice were analyzed with immunohistochemical assay. miR-142 was expressed at a lower level in human EC tumor samples than matched normal tissues, and its mRNA level in EC patients without metastasis was higher than that in patients with metastatic EC. Additionally, low-level miR-142 was closely linked with the poor prognosis of EC patients. miR-142 restricted ISK and HEC-1A cell proliferation. Targetscan and luciferase reporter assay proved the target relationship between miR-142 and CCND1. Moreover, high-level CCND1 was positively correlated with the poor prognosis of EC patients. Besides, miR-142 mimics restricted tumor growth in ISK xenografted mice, as well as inhibited the expression of Ki67 and CCND1 in excised tumors. miR-142 restricted EC proliferation by targeting CCND1.

主题词:Cell Proliferation/genetics*/细胞增殖/遗传学*

主题词:Cyclin D1/genetics*/细胞周期蛋白D1/遗传学*

主题词:Endometrial Neoplasms/genetics*/子宫内膜肿瘤/遗传学*

主题词:Endometrial Neoplasms/pathology*/子宫内膜肿瘤/病理学*

主题词:MicroRNAs/genetics*/RNAs/遗传学*

全文链接:请使用FMRS数据库下载该篇文章。

 

 

编号:27

题名:Oncogenic c-terminal cyclin D1 (CCND1) mutations are enriched in endometrioid endometrial adenocarcinomas.

致癌的c末端细胞周期蛋白D1CCND1)突变在子宫内膜样子宫内膜腺癌中富集

作者:Xu, J;Lin, DI

出处:PLoS One.2018,13(7):e0199688

IF2.776

摘要:  Cyclin D1 (CCND1) is a core cell cycle regulator and is frequently overexpressed in human cancers, often via amplification, translocation or post-transcription regulation. Accumulating evidence suggests that mutations of the CCND1 gene that result in nuclear retention and constitutive activation of CDK4/6 kinases are oncogenic drivers in cancer. However, the spectrum of CCND1 mutations across human cancers has not been systematically investigated. Here, we retrospectively mined whole-exome sequencing data from 124 published studies representing up to 29,432 cases from diverse cancer types and sites of origin, including carcinoma, melanoma, sarcoma and lymphoma/leukemia, via online tools to determine the frequency and spectrum of CCND1 mutations in human cancers and their associated clinico-pathological characteristics. Overall, in contrast to gene amplification, which occurred at a frequency of 4.8% (1,419 of 28,769 cases), CCND1 mutations were of very low frequency (0.5%, 151 of 29,432 cases) across all cancers, but were predominantly enriched in uterine endometrioid-type adenocarcinoma (6.5%, 30 of 458 cases) in both primary tumors and in advanced, metastatic endometrial cancer samples. CCND1 mutations in endometrial endometrioid adenocarcinoma occurred most commonly in the c-terminus of cyclin D1, as putative driver mutations, in a region thought to result in oncogenic activation of cyclin D1 via inhibition of Thr-286 phosphorylation and nuclear export, thereby resulting in nuclear retention and protein overexpression. Our findings implicate oncogenic c-terminal mutations of CCND1 in the pathogenesis of a subset of human cancers and provide a key resource to guide future preclinical and clinical investigations.

主题词:Adenocarcinoma/genetics*/腺癌/遗传学*

主题词:Adenocarcinoma/pathology*/腺癌/病理学*

主题词:Biomarkers, Tumor/genetics*/肿瘤标记, 生物学/遗传学*

主题词:Cyclin D1/genetics*/细胞周期蛋白D1/遗传学*

主题词:Endometrial Neoplasms/genetics*/子宫内膜肿瘤/遗传学*

主题词:Endometrial Neoplasms/pathology*/子宫内膜肿瘤/病理学*

主题词:Mutation*/突变*

全文链接:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6029777/

 

 

编号:28

题名:Cigarette smoke extract and isoprene resulted in the induction of apoptosis and autophagy in human placenta choriocarcinoma JEG-3 cells.

香烟烟雾提取物和异戊二烯诱导人胎盘绒毛膜癌JEG-3细胞凋亡和自噬

作者:Lee, HM;Choi, KC

出处:Environ Toxicol.2018,33(2):178-190

IF2.649

摘要:  In this study, the effects of cigarette smoke (CS) on the induction of apoptosis via reactive oxygen species (ROS) production and endoplasmic reticulum stress (ER stress) of JEG-3 human choriocarcinoma cells were examined to confirm the relationship between CS and placenta development. Upon TUNEL assay, CS extract (3R4F; 0.3 and 2.1 μM) increased JEG-3 apoptosis. Western blot assay revealed that the protein expressions of p53, Bax, and CCAAT-enhancer-binding protein homologous protein (CHOP) increased, while the levels of Bcl-2 were reduced following CS extract treatment. Moreover, 2',7'-dichlorofluorescein diacetate (DCFH-DA) assay revealed increased ROS production. Upon 3-(4-5-dimethylthiazol-2-yl)-2.5-dyhphenyltetrazolium bromide (MTT) assay, isoprene (IP), one of ingredients of CS, deceased JEG-3 cell viability (10-11 to 10-6 M). After based on the MTT assay, two IP concentrations of 10-11 and 10-8 M were selected and the protein expressions of cyclin D1, cyclin E1, p21, and p27 decreased in response to IP. Furthermore, IP showed the greatest increase in autophagy at 24 hours and further induction of cell death at 72 hours upon monodansylacadaverine and TUNEL assay. Western blot analysis confirmed the increase in autophagy markers, LC3β and p62, as well as the increase or decrease of apoptosis markers p53, Bax, CHOP, and Bcl-2 in response to its treatments. In addition to confirming increases in ROS through DCFH-DA, we also confirmed the expression of Nrf2, an antioxidant marker, and the expression of Kelch-like ECH-associated protein 1 (KEAP1), which specifically degrades Nrf2, by Western blot. Taken together, these results indicate that CS and IP may inhibit the development of placenta via activation of ROS by inducing apoptosis and autophagy by affecting the expression of KEAP1, which regulates Nrf2 expression.

主题词:Apoptosis/drug effects*/细胞凋亡/药物作用*

主题词:Autophagy/drug effects*/自噬/药物作用*

主题词:Butadienes/toxicity*/丁二烯类/毒性*

主题词:Cyclin D1/metabolism/细胞周期蛋白D1/代谢

主题词:Cyclin E/metabolism/细胞周期蛋白E/代谢

主题词:Hemiterpenes/toxicity*/半萜类/毒性*

主题词:Pentanes/toxicity*/戊烷类/毒性*

主题词:Uterine Neoplasms/metabolism/子宫肿瘤/代谢

全文链接:请使用FMRS数据库下载该篇文章。

 

 

编号:29

题名:Effect of monoacylglycerol lipase on the tumor growth in endometrial cancer.

单酰甘油脂酶对子宫内膜癌肿瘤生长的影响

作者:Li, X;Gao, S;Li, W;Liu, Z;Shi, Z;Qiu, C;Jiang, J

出处:J Obstet Gynaecol Res.2019,45(10):2043-2054

IF1.392

摘要:  AIM:Abnormal lipid metabolism plays a dual role in tumorigenesis, specifically in the occurrence and development of cancers. Monoacylglycerol lipase (MAGL), a hydrolase that is important for lipid metabolism, plays a vital role in different aspects of tumorigenesis. Many studies have shown that MAGL is highly elevated in a variety of cancers and plays an active role. However, its potential role in supporting endometrial cancer (EC) growth and progression has not yet been explored in depth. METHODS:Immunohistochemistry and quantitative real-time reverse transcription polymerase chain reaction were performed to estimate the protein and messenger RNA (mRNA) levels of MAGL in tumor tissues. Then, JZL184 and small interfering RNA (siRNA) were used to decrease the expression of MAGL in EC cells. The gene and protein expression levels of MAGL were measured using quantitative real-time PCR and western blotting, respectively. Additionally, the effect of MAGL on tumor growth in EC was detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide , cell cycle and western blotting assay in vitro. RESULTS:We found that MAGL was overexpressed in EC and was significantly correlated with surgical-pathological stage, myometrial invasion, number of pregnancies and body mass index. The growth and cell cycle progression of tumor cells were significantly impaired in vitro by the pharmacological and siRNA-mediated MAGL inhibition. In addition, MAGL inhibition seemed to repress two target genes, Cyclin D1 and Bcl-2. CONCLUSION:In summary, we have demonstrated that MAGL is involved in EC growth and progression. Our results suggest that targeting MAGL may be a novel and valid treatment for EC.

主题词:Adenocarcinoma/enzymology*/腺癌/酶学*

主题词:Cyclin D1/metabolism/细胞周期蛋白D1/代谢

主题词:Endometrial Neoplasms/enzymology*/子宫内膜肿瘤/酶学*

主题词:Monoacylglycerol Lipases/metabolism*/单酰基甘油酯脂酶类/代谢*

全文链接:请使用FMRS数据库下载该篇文章。

 

 

编号:30

题名:Long noncoding RNA H19 regulates HIF-1α/AXL signaling through inhibiting miR-20b-5p in endometrial cancer.

长非编码RNA H19通过抑制子宫内膜癌中的miR-20b-5p来调节HIF-1α/ AXL信号传导

作者:Zhu, H;Jin, YM;Lyu, XM;Fan, LM;Wu, F

出处:Cell Cycle.2019,18(19):2454-2464

IF3.699

摘要:  In a variety of cancers, long non-coding RNAs (lncRNAs) were believed to play important roles. Nevertheless, H19's possible molecular mechanism related to miR-20b-5p has not yet been explored in endometrial cancer. Differential lncRNAs in endometrial cancer were identified based on microarray analysis (GSE23339). In this research, in the first place, H19 expression was detected to be increased but miR-20b-5p to be decreased in endometrial cancer tissues and cells. Besides, H19 expression displayed a negative relationship to miR-20b-5p expression in endometrial cancer tissues. According to gain- and loss-of-function experiments of H19, like a ceRNA, H19 elevated AXL level and HIF-1α expression so as to stimulate the migration, proliferation and EMT process of endometrial cancer. Additionally, the knockdown of H19 slowed down tumor growth, promoted apoptosis and upregulated miR-20b-5p expression but lowered the expressions of HIF-1α, PCNA and AXL in vivo. Furthermore, H19 was also verified to stimulate the activity of endometrial cancer with AXL inhibitor BGB324 in vitro and in vivo. To sum up, H19 accelerates the tumor formation of endometrial cancer through the miR-20b-5p/AXL/HIF-1α signaling pathway, thereby providing a novel target for diagnosing and treating endometrial cancer.

主题词:Cell Proliferation/genetics/细胞增殖/遗传学

主题词:Endometrial Neoplasms/metabolism*/子宫内膜肿瘤/代谢*

主题词:Epithelial-Mesenchymal Transition/genetics/上皮细胞-间充质细胞转换/遗传学

主题词:Gene Expression Regulation, Neoplastic/genetics*/基因表达调控, 肿瘤/遗传学*

主题词:Hypoxia-Inducible Factor 1, alpha Subunit/metabolism*/缺氧诱导因子1, α亚基/代谢*

主题词:MicroRNAs/metabolism*/RNAs/代谢*

主题词:Proto-Oncogene Proteins/metabolism*/原癌基因蛋白质类/代谢*

主题词:RNA, Long Noncoding/metabolism*/RNA, 长链非编码/代谢*

主题词:Receptor Protein-Tyrosine Kinases/metabolism*/受体蛋白质酪氨酸激酶类/代谢*

主题词:Signal Transduction/genetics*/信号传导/遗传学*

全文链接:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6739051/

 

 

编号:31

题名:Immunohistochemical Expression of Different Subtypes of Cytokeratins by Endometrial Stromal Sarcoma.

子宫内膜间质肉瘤不同亚型细胞角蛋白的免疫组化表达

作者:Rahimi, S;Akaev, I;Marani, C;Chopra, M;Yeoh, CC

出处:Appl Immunohistochem Mol Morphol.2019,27(6):466-470

IF1.863

摘要:  Endometrial stromal sarcomas (ESS) are rare and understudied gynecologic mesenchymal neoplasms. These tumors can be confused with many other gynecologic and nongynecologic tumors due to their variegated morphologic appearance and nonspecific immunohistochemical profile. ESS can express cytokeratin (CK) and, therefore, may be misdiagnosed as carcinoma especially in extrauterine locations and when recurrence/metastasis is present. In this study, we investigated the expression of a wide spectrum of CKs consisting of AE1/3, CAM 5.2, HMCK, MNF116, CK5, CK6, CK7, CK8/18, CK14, CK17, CK19, and CK20 in 6 low-grade and 5 high-grade ESS. In addition, staining for estrogen receptor, progesterone receptor, CD10, and cyclin D1 was performed. Our results showed that CKs AE1/3, CAM 5.2, MNF116, and CK8/18 are more expressed in low-grade ESS, whereas high-grade ESS express more AE1/3 and CAM 5.2. In problematic cases, especially in recurrences or metastases, the immunohistochemical panel of antibodies AE1/3, MNF116, CAM 5.2, and CK8/18, together with other classic immunohistochemical markers CD10, cyclin D1, estrogen receptor, and progesterone receptor, may be helpful in the differential diagnosis between ESS and other gynecologic and nongynecologic malignancies.

主题词:Biomarkers, Tumor/metabolism*/肿瘤标记, 生物学/代谢*

主题词:Cyclin D1/metabolism/细胞周期蛋白D1/代谢

主题词:Endometrial Neoplasms/metabolism*/子宫内膜肿瘤/代谢*

主题词:Keratins/metabolism*/角蛋白类/代谢*

主题词:Sarcoma, Endometrial Stromal/metabolism*/肉瘤, 子宫内膜间质/代谢*

全文链接:请使用FMRS数据库下载该篇文章。

 

 

编号:32

题名:Assessment of HER-2/neu, с-MYC and CCNE1 gene copy number variations and protein expression in endometrial carcinomas.

评估子宫内膜癌中HER-2 / neu,с-MYCCCNE1基因拷贝数变异和蛋白表达

作者:Buchynska, LG;Brieieva, OV;Iurchenko, NP

出处:Exp Oncol.2019,41(2):138-143

摘要:  AIM:To analyze copy number variations of HER-2/neu, c-MYC and CCNE1 oncogenes and their protein expression in endometrioid endometrial carcinomas in relation to the degree of tumor progression and presence of a family history of cancer in cancer patients. MATERIALS AND METHODS:The study was conducted on endometrial cancer (EC) samples from 68 patients with I-II FIGO stages of disease. Copy number analysis of HER-2/neu, c-MYC and CCNE1 genes was performed by quantitative PCR. Protein expression was analyzed using immunohistochemistry. RESULTS:Assessment of copy number variations of HER-2/neu, c-MYC and CCNE1 genes revealed their amplification in the tumors of 18.8, 25.0?and 14.3% of EC patients, respectively. High expression of corresponding proteins was detected in 14.6, 23.5 and 65.6% of patients, respectively. It was established that HER-2/neu gene amplification is more common in the group of tumors of low differentiation grade than in moderate grade EC (35.7 and 5.5% of cases, respectively, p < 0.05). Also, high expression of c-Myc protein was more frequently observed in low differentiated tumors compared to the moderately differentiated EC (36.6?and 13.2% of cases, respectively, p < 0.05). Expression of HER-2/neu and cyclin E proteins was found to be dependent on the depth of tumor invasion into the myometrium. High expression of HER-2/neu protein was observed in 25.0?and 4.1% of EC patients with tumor invasion > ½ and < ½ of the myometrium, respectively, and cyclin E - in 86.7 and 46.6% of cases, respectively, p < 0.05. It was shown that among patients with a family history of cancer, a larger proportion of cases with high expression of c-Myc protein was observed compared to the group of patients with sporadic tumors (43.8 and 17.3%, respectively; p < 0.05). CONCLUSIONS:Amplification of HER-2/neu gene, along with high expression of c-Myc, HER-2/neu and cyclin E proteins, are associated with such indices of tumor progression as a low differentiation grade and deep myometrial invasion, suggesting the potential possibility of including these markers in the panel for determining the molecular EC subtype associated with an aggressive course of the disease. In a certain category of EC patients, there is a relationship between a family history of cancer and high expression of c-Myc protein.

主题词:Carcinoma, Endometrioid/genetics*/, 子宫内膜样/遗传学*

主题词:Cyclin E/genetics*/细胞周期蛋白E/遗传学*

主题词:Endometrial Neoplasms/genetics*/子宫内膜肿瘤/遗传学*

主题词:Oncogene Proteins/genetics*/癌基因蛋白质类/遗传学*

主题词:Proto-Oncogene Proteins c-myc/genetics*/原癌基因蛋白质c-myc/遗传学*

主题词:Receptor, ErbB-2/genetics*/受体, erbB-2/遗传学*

全文链接:

https://exp-oncology.com.ua/article/12973/assessment-of-em-her-2-neu-em-em-s-myc-em-and-em-ccne1-em-gene-copy-number-variations-and-protein-expression-in-endometrial-carcinomas

 

 

编号:33

题名:Utility of YWHAE fluorescent in-situ hybridisation in mesenchymal tumors of uterus- An initial experience from tertiary oncology centre in India.

YWHAE荧光原位杂交技术在子宫间质肿瘤中的应用-来自印度三级肿瘤中心的初步经验

作者:Verma, A;Menon, S;Rekhi, B;Pai, T;Maheshwari, A;Ghosh, J;Gupta, S;Deodhar, K

出处:Indian J Cancer.2019,56(4):335-340

IF0.765

摘要:  Background:Endometrial stromal sarcoma (ESS) is a common uterine mesenchymal malignancy. According to World Health Organisation (WHO) 2014 classification, ESSs are further subdivided into low-grade ESS (LGESS) and high-grade ESS (HGESS). HGESS is defined by the presence of YWHAE gene rearrangement and has a poorer prognosis compared to LGESS. METHODS:Twenty-four cases comprising of 16 endometrial stromal sarcoma and 8 lesions mimicking ESS were retrieved from the archives of the Department of Pathology and subjected to fluorescent in situ hybridization (FISH) analysis for YWHAE gene rearrangement. Immunohistochemistry for CD10, ER, PR, Cyclin D1, SMA, H-Caldesmon, Desmin, Ki-67, and Pan Cytokeratin was performed. RESULTS:Two cases with histological features similar to HGESS were positive for YWHAE gene rearrangement while 1 was indeterminate. No cases of LGESS and histological mimics of ESS were positive for this rearrangement. CONCLUSIONS:HGESSs are defined by the presence of YWHAE rearrangement. These tumors present at higher stage and have poorer prognosis. They may not respond to hormonal therapy and may be treated with chemotherapy. Cyclin D1 though not specific remains a sensitive tool to triage endometrial stromal sarcomas for this FISH study.

主题词:14-3-3 Proteins/genetics*/14-3-3蛋白质类/遗传学*

主题词:Cyclin D1/metabolism*/细胞周期蛋白D1/代谢*

主题词:Mesenchymal Stem Cells/pathology*/间质干细胞/病理学*

主题词:Sarcoma, Endometrial Stromal/diagnosis*/肉瘤, 子宫内膜间质/诊断*

主题词:Uterine Neoplasms/diagnosis*/子宫肿瘤/诊断*

全文链接:

http://www.indianjcancer.com/article.asp?issn=0019-509X;year=2019;volume=56;issue=4;spage=335;epage=340;aulast=Verma

 

 

编号:34

题名:Regulation of Cell Cycle Regulatory Proteins by MicroRNAs in Uterine Leiomyoma.

MicroRNA在子宫平滑肌瘤中对细胞周期调节蛋白的调节

作者:Chuang, TD;Khorram, O

出处:Reprod Sci.2019,26(2):250-258

IF2.559

摘要:  The objective of this study was to determine whether miR-93, miR-29c, and miR-200c, which we previously reported to be downregulated in leiomyomas, target cell cycle regulatory proteins that influence cell proliferation. Based on TargetScan algorithm 3 cell cycle regulatory proteins namely, E2F transcription factor 1 (E2F1), Cyclin D1 (CCND1) and CDK2 which were predicted to be targets of these miRNAs were ?further analyzed. In 30 hysterectomy specimens, we found the expression of E2F1 and CCND1 messenger RNA (mRNA) was increased in leiomyoma as compared to matched myometrium, with no significant changes in CDK2 mRNA levels. There was a significant increase in the abundance of all 3 proteins in leiomyoma in comparison with matched myometrium. Using luciferase reporter assay, we demonstrated E2F1 and CCND1 are targets of miR-93 and CDK2 is a target of miR-29c and miR-200c. We confirmed these findings through transfection studies in which transfection of primary leiomyoma cells with miR-93 resulted in a significant decrease in the expression of E2F1 and CCND1 mRNA and protein levels, whereas knockdown of miR-93 had the opposite effect. Similarly, overexpression of miR-29c and miR-200c in leiomyoma cells inhibited the expression of CDK2 protein and mRNA, whereas knockdown of this microRNAs (miRNA) had the opposite effect. Transfection of miR-29c, miR-200c, and miR-93 in primary leiomyoma cells resulted in a time-dependent inhibition of cell proliferation and cell motility. These results collectively indicate that the 3 miRNAs known to be downregulated in fibroid tumors are critical in regulation of cell proliferation because of their effects on 3 key cell cycle regulatory proteins, which are overexpressed in uterine leiomyomas.

主题词:Cell Cycle Proteins/metabolism*/细胞周期蛋白质类/代谢*

主题词:Cyclin D1/细胞周期蛋白D1

主题词:Gene Expression Regulation, Neoplastic*/基因表达调控, 肿瘤*

主题词:Leiomyoma/metabolism*/平滑肌瘤/代谢*

主题词:MicroRNAs/metabolism*/RNAs/代谢*

主题词:Uterine Neoplasms/metabolism*/子宫肿瘤/代谢*

全文链接:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6728566/

 

 

编号:35

题名:1,25 Dihydroxyvitamin D3 Enhances the Antifibroid Effects of Ulipristal Acetate in Human Uterine Fibroids.

1,25二羟维生素D3增强子宫肌瘤中醋酸乌头酸的抗纤维化作用

作者:Ali, M;Shahin, SM;Sabri, NA;Al-Hendy, A;Yang, Q

出处:Reprod Sci.2019,26(6):812-828

IF2.559

摘要:  BACKGROUND:Both European and American trials showed superior effect of ulipristal acetate (UPA) to placebo. However, the latter, which included black patients with known higher vitaminD3 deficiency risk, showed lower rate of amenorrhea responders and insignificant uterine fibroid (UF) size reduction. Our objective is to investigate whether adding vitamin D3 to UPA can enhance UPA potency on UF phenotype in vitro. METHODS:We screened the antiproliferative effect of different (UPA/vitaminD3) combinations on UF cell proliferation using dimethylthiazolyl diphenyltetrazolium bromide assay. Cells then were treated with UPA 100 nM in the presence or absence of vitamin D3 100 nM, and expression level of several markers related to proliferation, apoptosis, fibrosis, inflammation, and angiogenesis was measured on RNA or at protein level using quantitative real-time polymerase chain reaction, Western blot, immunofluorescence, or multiplex enzyme-linked immunosorbent assay techniques. RESULTS:Significant dose- and time-dependent growth inhibitory effects of UPA/vitamin D3 combinations were observed compared to untreated cells at 2 and 4 days (P < .05). Importantly, vitamin D3/UPA combination significantly reduced cell proliferation as compared to UPA at 2, 4, 6, and 8 days (P < .05). Combination treatment significantly decreased protein expression of proliferation markers Ki-67, PCNA, and CyclinD1 by more than 50% compared to UPA (P < .05) along with a significant increase in apoptosis induction. Combination treatment resulted in a 2-fold decrease in protein levels of extracellular matrix markers collagen-1 and fibronectin besides pro-fibrogenic cytokine transforming growth factor β3 (P < .05). Moreover, it significantly decreased the production of pro-inflammatory cytokines interleukins 6, 8, 1α, and 1β compared to UPA (P < .05). CONCLUSION:Combination of vitamin D3 with UPA exhibits additional and orchestrated anti-UF effects, therefore might offer a more favorable clinical option.

主题词:Cyclin D1/analysis/细胞周期蛋白D1/分析

主题词:Leiomyoma/drug therapy*/平滑肌瘤/药物疗法*

主题词:Norpregnadienes/administration & dosage*/去甲孕甾二烯类/给药与剂量*

主题词:Uterine Neoplasms/drug therapy*/子宫肿瘤/药物疗法*

主题词:Vitamin D/analogs & derivatives*/维生素D/类似物与衍生物*

全文链接:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6728560/

 

 

 

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