MiR-101 reduces cell proliferation and invasion and enhances apoptosis in endometrial cancer via regulating PI3K/Akt/mTOR.

Abstract

PI3K/Akt/mTOR signaling pathway plays an important role in tumor development. mTOR overexpression and PI3K/ Akt/mTOR signaling pathway enhancement were found in endometrial cancer (EC). MiR-101 was found downregulated in EC. Bioinformatics analysis showed the binding site between miR-101 and the 3'-UTR of mTOR mRNA. This study investigated the role of miR-101 in affecting EC proliferation, apoptosis, and invasion, and mediating mTOR expression. EC tumor tissue and normal endometrial tissue were collected from Jinan maternity and child care hospital. MiR-101 and mTOR expressions were detected. The targeted relationship between miR-101 and mTOR was tested by dual-luciferase reporter gene assay. MiR-101, mTOR, p-mTOR, and p-4EBP1 expressions between HEEC and HEC-1A cells were compared. HEC-1A cells were cultured in vitro and divided into five groups, including miR-NC, miR-101 mimic, si-NC, si-mTOR, and miR-101 + si-mTOR. mTOR, p-mTOR, and p-4EBP1 expressions were compared. Cell apoptosis was evaluated by flow cytometry. Cell malignant proliferation was evaluated by colony formation assay. Cell invasion was determined by Transwell assay. MiR-101 and mTOR expressions significantly declined in EC tissue compared with normal endometrium. MiR-101 showed targeted relationship with mTOR. MiR-101 reduced, while mTOR, p-mTOR, and p-4EBP1 levels elevated in HEC-1 cells compared with HEEC cells. MiR-101 mimic and/or si-mTOR transfection obviously reduced mTOR, p-mTOR, and p-4EBP1 expressions, decreased colony formation, decreased invasion, and enhanced apoptosis in HEC-1A cells. MiR-101 downregulated and mTOR elevated in EC tissue. MiR-101 decreased HEC-1A cell proliferation and invasion, and upregulated apoptosis through targeting mTOR to attenuate PI3K/Akt/ mTOR signaling pathway activity.