miR-1264 Exacerbates Proliferation, Migration and Invasion of Endometrial Cancer Cells by Targeting MSH2.

Abstract

Accumulating studies have revealed that microRNAs serve significant regulatory for endometrial carcinoma (EC) tumorigenesis and progression. The specific objective of this investigation is to seek the potential function of miR-1264 in EC and clarified the underlying mechanism. Determination of miR-1264 and MSH2 expression in EC tissues or cell lines was performed by RT-qPCR and/or western blot assay. The malignant behaviors of EC cells were verified by CCK-8 assay, EdU staining, wound healing assay and Transwell assay, respectively. Besides, the interaction between miR-1264 and MSH2 was verified by dual-luciferase reporter assay and RNA immunoprecipitation assay. MiR-1264 exhibited high levels in EC tissues and has been found to be correlated with a poor prognosis in EC patients. Functionally, silencing miR-1264 resulted in inhibiting the aggressiveness behaviors of HEC-1 A and KLE cells, while forced miR-1264 expression executed opposite effects. Mechanistically, miR-1264 directly targeted and suppressed MSH2 expression. Functional rescue experiments further validated that overexpression of MSH2 diminished malignant behaviors of EC cells and greatly reversed the promoting effects of miR-1264 on the malignant behaviors of EC cells. MiR-1264 acted as an oncogene in EC, promoting aggressiveness behaviors of EC cells by inhibiting MSH2. This study provided novel insights into anti-cancer treatment and a theoretical basis for potential therapeutic targets of EC.