MiR-326 regulates the proliferation and apoptosis of endometrial cancer by targeting Bcl-2.

Abstract

MiR-326 has been investigated to be correlated with multiple types of malignancies; however, the role of miR-326 in endometrial cancer (EC) remains rarely reported. The aim of our research is to investigate the functions of miR-326 in EC and the potential molecular mechanism. RT-qPCR was performed to compare the expression of miR-326 and Bcl-2 in normal endometrial epithelial cell line (End1/e6e7) and EC cells lines (HEC-1A, Ishikawa), respectively. Bioinformatic analysis and luciferase assay verified the relationship between miR-326 and the 3'-UTR of Bcl-2. 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay, soft agar colony formation assay and the flow cytometry were performed to investigate the functions of miR-326 and Bcl-2 on proliferation and apoptosis in EC. Western blotting was employed to explore the expression of Bcl-2, Bcl2-associated X (Bax) and caspase-3. The expression of miR-326 decreased in EC cell lines compared to normal endometrial epithelial cell line, while Bcl-2 expression was increased in EC cells. Results of MTT and soft agar colony formation assays showed that miR-326 suppressed proliferation in EC cells. In addition, flow cytometry revealed that miR-326 promoted apoptosis in EC cells. Western blotting showed that silencing miR-326 promoted the expression of Bcl-2. Bioinformatics analysis and luciferase assay verified the 3'-UTR of Bcl-2 was a target of miR-326. Furthermore, MTT assay, soft agar colony formation assay and the flow cytometry proved that miR-326 acts as tumor suppressor via inhibiting the expression of Bcl-2. MiR-326 acts as a cancer suppressor to inhibit proliferation and promote apoptosis via targeting Bcl-2 axis in EC.