miR­92b promotes autophagy and suppresses viability and invasion in breast cancer by targeting EZH2.

MicroRNAs (miRs) are a small non-coding RNA family with a length of 18-22 nucleotides. They are able to regulate gene expression by either triggering target messenger RNA degradation or by inhibiting mRNA translation. Enhancer of zeste homolog 2 (EZH2) is the core enzymatic subunit of polycomb repressor complex 2 and is responsible for the trimethylation of histone 3 on lysine 27 (H3K27me3); it is also able to silence a bundle of tumor suppressor genes through promoter binding. However, little is known regarding the effect of miR­92b on cell autophagy, viability and invasion as well as how it interacts with EZH2. The present study investigated the major role of miR­92b in the autophagy, viability and invasion of breast cancer. It was revealed that in MCF­7 and MDA­MB­453 cells, the expression of miR­92b promoted autophagy induced by starvation and rapamycin treatment. The results of in vitro experiments results demonstrated that miR­92b inhibited breast cancer cell viability, invasion and migration. To further elucidate the regulatory mechanisms of miR­92b in autophagy, a dual luciferase reporter assay was performed to determine whether miR­92b targeted the EZH2 gene. The expression of miR­92b was negatively correlated to EZH2 mRNA expression in breast cancer. Depletion of EZH2 induced phenocopied effects on miR­92b overexpression, thereby demonstrating its importance in autophagy. These results indicated that miR­92b may serve an important role in breast cancer in controlling autophagy, viability and invasion. The present study indicated that miR­92b and EZH2 may serve as potential biomarkers for cancer detection and highlighted their possible therapeutic implications.