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

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.