MicroRNA-139-3p Inhibits The Growth And Metastasis Of Ovarian Cancer By Inhibiting ELAVL1.

Onco Targets Ther

Infertility Center, Department of Gynaecology and Obstetrics, Qilu Hospital of Shandong University, Jinan, Shandong 250012, People's Republic of China.

Published: November 2019

Background: The aberrant expression of microRNA-139-3p (miR-139-3p) has been recently involved in the development of multiple tumor types, but its function in ovarian cancer remains not well investigated. In this study, we mainly investigated the function of miR-139-3p in the progression of ovarian cancer.

Methods: The levels of miR-139-3p in ovarian cancer cells and tissues were detected using quantitative real-time-PCR (qRT-PCR) assay. The proliferation, colony formation, migration and invasion of ovarian cancer cell were determined, respectively. A luciferase reporter assay was used to confirm ELAV Like RNA Binding Protein 1 (ELAVL1) was a target gene of miR-139-3p. The expression of ELAVL1 was detected using Western blotting and immunofluorescence staining assay. The roles of miR-139-3p on the growth and metastasis of ovarian cancer cell in vivo were explored using transplanted tumor model and experimental lung metastasis model.

Results: MiR-139-3p was down-regulated in ovarian cancer tissues and ovarian cancer cell lines (SK-OV-3, A2780 and OVCAR-3). Overexpression of miR-139-3p decreased the growth, colony formation, migration and invasiveness of SK-OV-3 and OVCAR-3 cells. Moreover, overexpression of miR-139-3p reduced the growth and lung metastasis of ovarian cancer cells in vivo. The luciferase reporter gene assay indicated that ELAVL1 was a target of miR-139-3p and its expression was negatively regulated by miR-139-3p. Furthermore, the expression of ELAVL1 was inversely correlated with miR-139-3p level in ovarian cancer tissue.

Conclusion: Taken together, we demonstrated that miR-139-3p regulated ovarian cancer growth and metastasis by modulating the expression of ELAVL1.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6842313PMC
http://dx.doi.org/10.2147/OTT.S210739DOI Listing

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