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Anti-Condyloma acuminata mechanism of microRNAs-375 modulates HPV in cervical cancer cells via the UBE3A and IGF-1R pathway

机译:microRNAs-375的抗尖锐湿疣机制通过UBE3A和IGF-1R途径调节子宫颈癌细胞中的HPV

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摘要

The present study aimed to identify the probable anti-Condyloma acuminata (CA) mechanism of microRNA-375 (miRNA-375) in human papillomavirus (HPV). Firstly, the overexpression of miRNA-375 significantly suppressed cell proliferation, increased lactate dehydrogenase activity and induced apoptosis in HPV-18(+) cervical cancer cells. The overexpression of miRNA-375 significantly increased caspase-3 and caspase-9 activities, induced B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X protein, tumor protein 53 and cyclin-dependent kinase inhibitor 1 protein expression and suppressed cyclin D1 and survivin protein expression in HPV-18(+) cervical cancer cells. The overexpression of miRNA-375 significantly suppressed the levels of protein expression of ubiquitin-protein ligase E3A (UBE3A) and Insulin-like growth factor-1 receptor (IGF-1R) in HPV-18(+) cervical cancer cells. To conclude, it was identified that the probable anti-CA mechanism of miRNA-375 modulates HPV through the UBE3A and IGF-1R pathway in cervical cancer cells.
机译:本研究旨在确定人类乳头瘤病毒(HPV)中microRNA-375(miRNA-375)的可能的尖锐湿疣(CA)机制。首先,miRNA-375的过表达显着抑制了HPV-18(+)宫颈癌细胞的细胞增殖,增加了乳酸脱氢酶的活性并诱导了细胞凋亡。 miRNA-375的过表达显着增加caspase-3和caspase-9活性,诱导B细胞淋巴瘤2(Bcl-2)/ Bcl-2相关X蛋白,肿瘤蛋白53和细胞周期蛋白依赖性激酶抑制剂1蛋白的表达和抑制HPV-18(+)宫颈癌细胞中cyclin D1和survivin蛋白的表达。 miRNA-375的过表达显着抑制了HPV-18(+)宫颈癌细胞中泛素-蛋白连接酶E3A(UBE3A)和胰岛素样生长因子-1受体(IGF-1R)的蛋白表达水平。总之,已确定miRNA-375的可能的抗CA机制通过子宫颈癌细胞中的UBE3A和IGF-1R途径调节HPV。

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