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细胞周期蛋白依赖性激酶在miR-193a-5p调控卵巢癌细胞增殖及上皮间质转化中的作用

[The role of cyclin-dependent kinases in miR-193a5p regulating ovarian cancer cell proliferation and epithelial mesenchymal transformation].

作者信息

Yang Zun-Jing, DU Xian-Ling

机构信息

Department of Oncology, Enshi Central Hospital, Enshi 445000, China.

出版信息

Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2020 Mar;36(2):176-179. doi: 10.12047/j.cjap.5888.2020.039.

Abstract

To investigate whether miR-193a-5p targets CDK14 and regulates the proliferation and epithelial-mesenchymal transition (EMT) of ovarian cancer cell line OVAC. TargetScanHuman was used to analyze the match between miR-193a-5p and CDK14, and then miRNA assay was used to detect whether miR-193a-5p targeting CDK14; miR-193a-5p mimics overexpression or miR-193a-5p inhibitor knockdown in the case of low miR-193a-5p, the expression levels of CDK14, EMT-related proteins E-cadherin, vimentin, fibronectin and N-cadherin were detected by immunoblotting, and the proliferation of ovarian cancer cells OVAC was detected by CCK-8, and the cell viability of cancer cell OVAC was detected by MMT. miR-193a-5p targeted the 3'UTR of CDK14; after overexpression of miR-193a-5, the expression of CDK14 was decreased, the expression of EMT-related protein E-cadherin was increased, and the expressions of vimentin, fibronectin and N-cadherin were decreased. The proliferation and cell viability of ovarian cancer cell line OVAC were increased. Meanwhile, after knocking down miR-193a-5p, the expression of CDK14 was increased, and the expression of EMT-related protein E-cadherin was decreased, while the expression levels of vimentin, fibronectin and N-cadherin were increased, and the proliferation and cell viability of ovarian cancer cell line OVAC were decreased. miR-193a-5p reduces the proliferation, cell viability and EMT of ovarian cancer cell line OVAC by targeting the 3 'UTR of CDK14.

摘要

研究miR-193a-5p是否靶向细胞周期蛋白依赖性激酶14(CDK14)并调节卵巢癌细胞系OVAC的增殖和上皮-间质转化(EMT)。使用TargetScanHuman分析miR-193a-5p与CDK14之间的匹配情况,然后采用miRNA检测法检测miR-193a-5p是否靶向CDK14;在miR-193a-5p低表达的情况下,通过转染miR-193a-5p模拟物进行过表达或转染miR-193a-5p抑制剂进行敲低,采用免疫印迹法检测CDK14、EMT相关蛋白E-钙黏蛋白、波形蛋白、纤连蛋白和N-钙黏蛋白的表达水平,采用CCK-8法检测卵巢癌细胞系OVAC的增殖情况,采用MTT法检测癌细胞系OVAC的细胞活力。miR-193a-5p靶向CDK14的3'非翻译区(3'UTR);过表达miR-193a-5后,CDK14的表达降低,EMT相关蛋白E-钙黏蛋白的表达增加,波形蛋白、纤连蛋白和N-钙黏蛋白的表达降低。卵巢癌细胞系OVAC的增殖和细胞活力增加。同时,敲低miR-193a-5p后,CDK14的表达增加,EMT相关蛋白E-钙黏蛋白的表达降低,而波形蛋白、纤连蛋白和N-钙黏蛋白的表达水平增加,卵巢癌细胞系OVAC的增殖和细胞活力降低。miR-193a-5p通过靶向CDK14的3'UTR降低卵巢癌细胞系OVAC的增殖、细胞活力和EMT。

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