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miR-101 regulates expression of EZH2 and contributes to progression of and cisplatin resistance in epithelial ovarian cancer

机译:miR-101调节上皮性卵巢癌EZH2的表达并促进顺铂耐药和顺铂耐药

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In order to determine the expression pattern of miR-101 in epithelial ovarian neoplasms and assess the functions and mechanism of miR-101 in tumorigenesis, we detected the expression of miR-101 and zeste homolog 2 (EZH2) in normal, benign, and malignant ovarian tissues and used miR-101 lentivirus infection to increase miR-101 expression in ovarian cancer cells and drug-resistant cancer cells. We found that miR-101 was underexpressed in epithelial ovarian cancer tissues, which significantly correlated with poor cell differentiation, advanced International Federation of Gynecology and Obstetrics (FIGO) stages, and ovarian cancer cell cisplatin resistance. miR-101 overexpression decreased the expression of EZH2, reduced proliferation and migration of ovarian cancer cells, and resensitized drug-resistant cancer cells to cisplatin-induced cytotoxicity, suggesting the important role miR-101 plays in ovarian cancer that may be associated with its function as a regulator targeting EZH2. Our findings show the potential of miR-101 as a diagnostic marker and new therapeutic target for patients with epithelial ovarian cancer.
机译:为了确定miR-101在卵巢上皮肿瘤中的表达模式并评估miR-101在肿瘤发生中的功能和机制,我们检测了正常,良性和恶性肿瘤中miR-101和zeste同源物2(EZH2)的表达。卵巢组织并使用miR-101慢病毒感染来增加miR-101在卵巢癌细胞和耐药性癌细胞中的表达。我们发现,miR-101在上皮性卵巢癌组织中表达不足,这与细胞分化差,国际妇产科联合会(FIGO)晚期以及卵巢癌细胞的顺铂耐药性显着相关。 miR-101的过表达降低了EZH2的表达,降低了卵巢癌细胞的增殖和迁移,并使耐药性细胞对顺铂诱导的细胞毒性重新敏感,这表明miR-101在卵巢癌中可能起重要作用,可能与其功能有关作为针对EZH2的调节剂。我们的发现表明,miR-101可能是上皮性卵巢癌患者的诊断标志物和新的治疗靶标。

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