microrna 302b-3p/302c-3p/302d-3p inhibits epithelial–mesenchymal transition and promotes apoptosis in human endometrial carcinoma cells

Yibing Li, Jianing Huo, Xin Pan, Cuicui Wang, Xiaoxin Ma Department of Obstetrics and Gynecology, Shengjing Hospital of China Medical University, Shenyang, Liaoning, People’s Republic of China Background: Studies have shown that the microRNA miR-302 can affect the proliferation, migration and cell cycle progression of endometrial carcinoma (EC). miR-302 clusters have been shown to play an important role in the proliferation and differentiation of cancer cells and in their tumorigenicity.Subjects and methods: In this study, we detected the expression of genes through quantitative reverse transcription polymerase chain reaction (qRT-PCR). We detected the expression of proteins through Western blot. The Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) double-staining assay were used to detect the ability of miR-302b-3p/302c-3p/302d-3p to affect the cell apoptosis. The CCK-8 were used to detect the ability of miR-302b-3p/302c-3p/ 302d-3p to affect the cell proliferation. The Cell cycle analysis were used to detect the ability of miR-302b-3p/302c-3p/302d-3p to affect the cell cycle. Finally, the wound healing assay was used to detect the ability of miR-302b-3p/302c-3p/302d-3p to impact cell migration.Results: We found that miR-302b-3p/302c-3p/302d-3p of the miR-302 cluster was downregulated in EC, and it altered the epithelial–mesenchymal transition (EMT) process in the EC cell lines Ishikawa and HEC-1A. Western blot and the Annexin V- FITC/PI double-staining assay were used to detect the ability of miR-302b-3p/302c-3p/302d-3p to promote the apoptosis of Ishikawa and HEC-1A cells. In addition, qRT-PCR results showed that overexpression of miR-302b-3p/302c-3p/302d-3p significantly inhibited the expression of ZEB1, suppressed the expression of Bcl-2 and promoted the expression of BAX. The overexpression of miR-302b-3p/302c-3p/302d-3p inhibited the proliferation and migration of Ishikawa and HEC-1A cells. Cell cycle analysis showed that miR-302b-3p/302c-3p/302d-3p arrested cell cycle progression in the G0/G1 phase.Conclusion: All results showed that miR-302b-3p/302c-3p/302d-3p can be used as a tumor suppressor in EC and is expected to be a new target for the treatment of EC. Keywords: endometrial carcinoma, miR-302b-3p, miR-302c-3p, miR-302d-3p, EMT, cell apoptosis