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MiR‐326 regulates the proliferation and apoptosis of endometrial cancer by targeting Bcl‐2
Author(s) -
Cai Lily,
Chen JuanJuan,
Deng FuMou,
Wang Lei,
Chen Yu
Publication year - 2021
Publication title -
journal of obstetrics and gynaecology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.597
H-Index - 50
eISSN - 1447-0756
pISSN - 1341-8076
DOI - 10.1111/jog.14572
Subject(s) - flow cytometry , apoptosis , mtt assay , blot , cell culture , microbiology and biotechnology , cell growth , luciferase , cancer research , biology , transfection , gene , biochemistry , genetics
Aim 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. Methods 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. Results 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. Conclusion MiR‐326 acts as a cancer suppressor to inhibit proliferation and promote apoptosis via targeting Bcl‐2 axis in EC.