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
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.
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.