miR-199a-5p promotes proliferation and metastasis and epithelial-mesenchymal transition through targeting PIAS3 in cervical carcinoma

miR-199a-5p通过靶向PIAS3促进宫颈癌增殖转移及上皮间质转化

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Abstract

Cervical carcinoma is the second most frequent gynecological malignancies in females worldwide. The objective of this study was to investigate the role of miR-199a-5p and protein inhibitor of activated signal transducer and activators of transcription 3 (PIAS3) in cervical carcinoma. Quantitative reverse transcription polymerase chain reaction was utilized to detect miR-199a-5p and PIAS3 expression in cervical carcinoma tissues and cells. 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide Kit, transwell assay were used to explore the biological functions of miR-199a-5p in cervical carcinoma. Western blot analysis was applied to determine the expression level of epithelial-mesenchymal transition (EMT)-associated proteins and PIAS3 expression. The relationship between miR-199a-5p and PIAS3 was verified by luciferase activity reporter assay. We found that miR-199a-5p was upregulated in cervical carcinoma tissues and cell lines, and overexpression of miR-199a-5p promoted cell proliferation and metastasis in cervical carcinoma. In addition, Western blot analysis indicated that the enforced upregulation of miR-199a-5p enhanced mesenchymal markers vimentin and N-cadherin expressions, whereas reduced epithelial marker E-cadherin expressions. miR-199a-5p directly targeted PIAS3 and negatively regulated PIAS3 level in cervical carcinoma cells. And upregulation of PIAS3 reversed the effects of miR-199a-5p in cervical carcinoma. Collectively, our data provide evidence for miR-199a-5p function in cervical carcinoma growth, EMT, and metastasis; it may be act as a therapeutic strategy target for patients with cervical carcinoma.

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