MicroRNA-424/E2F6 feedback loop modulates cell invasion, migration and EMT in endometrial carcinoma
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Zheng Lu1, Zhou Nian1, Zhang Jingjing1, Luo Tao1 and Li Quan1
1Department of Gynaecology, The First Affiliated Hospital of Zunyi Medical College, Zunyi, Guizhou 563000, P.R. China
Li Quan, email: [email protected]
Keywords: miR-424; E2F6; endometrial carcinoma
Received: August 23, 2017 Accepted: October 28, 2017 Published: December 13, 2017
Our previous study explored the roles of microRNA-424 (miR-424) in the development of endometrial carcinoma (EC) and analyzed the miR-424/E2F7 axis in EC cell growth. In this study, we investigated the status of miR-424 in human endometrial cancer tissues, which were collected from a cohort of Zunyi patients. We found that the expression level of miR-424 was associated with clinical tumor stage, cell differentiation, lymph node metastasis and cell migration ability. Cell function experiments demonstrated that miR-424 overexpression suppressed the invasion and migration abilities of endometrial carcinoma cells in vitro. Bioinformatic predictions and dual-luciferase reporter assays suggested E2F6 as a possible target of miR-424. RT-PCR and western blot assays demonstrated that miR-424 transfection reduced the expression level of E2F6, while inhibiting miR-424 with ASO-miR-424 (antisense oligonucleotides of miR-424) increased the expression level of E2F6. Cell function experiments indicated that E2F6 transfection rescued the EC cell phenotype induced by miR-424. In addition, we also found that E2F6 negatively regulated miR-424 expression in EC cells. In summary, our results demonstrated that the miR-424/E2F6 feedback loop modulates cell invasion, migration and EMT in EC and that the miR-424/E2Fs regulation network may serve as a new and potentially important therapeutic target in EC.
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