miR-101-3p induces autophagy in endometrial carcinoma cells by targeting EZH2.

OBJECTIVE: This study aimed to investigate the effect of miR-101-3p on autophagy in endometrial carcinoma (EC) cells and the connection between miR-101-3p and EZH2.

METHODS: The expression levels of miRNAs were analyzed by microarray. The expression level of autophagy related proteins was measured by western blot. The mRNA expression level of beclin-1 was determined by qRT-PCR. Autophagy in EC cells was traced by GFP-LC3 fusion protein and observed by fluorescence microscopy. The number of autophagic vacuoles was determined by transmission electron microscopy (TEM). A luciferase reporter assay was utilized to assess the target relationship between miR-101-3p and EZH2.

RESULTS: The expression level of miR-101-3p in EC tissues was lower than in normal tissues. miR-101-3p upregulated the expression levels of the autophagy-related proteins LC3-II and beclin-1 in EC cells in a time- and dose-dependent manner. Overexpression of miR-101-3p and silencing of EZH2 both promoted autophagy in EC cells. Luciferase reporter assays verified that miR-101-3p inhibited EZH2 expression by binding to its 3'-UTR region.

CONCLUSION: miR-101-3p promoted autophagy in EC cells by downregulating the expression of EZH2, and it induced autophagy in EC cells by suppressing EZH2 expression. Inhibition of miR-101-3p could reduce its autophagy induction effect on EC cells.