MiR-502 mediates esophageal cancer cell TE1 proliferation by promoting AKT phosphorylation

Abstract

Esophageal cancer is one of the most common cancers in the world and esophageal squamous cell carcinoma is one of the two main types in esophageal cancer. MicroRNA is a small non-coding RNA molecule functions in many different cancers including esophageal cancer. We found miR-502 was up-regulated in esophageal tissues, which indicated miRNA-502 may play important roles in esophageal cancer. In this study, we used esophageal cancer cell line TE1 as an in vitro model for investigating the role of miR-502 in promoting the proliferation of the cancer cells. We found that overexpressing miR-502 in TE1 cells promoted the proliferation and inhibited the apoptosis induced by dox. Down-regulating miR-502 made the opposite phenomenon. Furthermore, western blot showed that miR-502 enhanced the phosphorylation levels of AKT pathways, which may be the mechanism of the overgrowth for esophageal cancer cell. Our data provide the evidence of a role for miR-502 in the regulation the proliferation of esophageal cancer cell through promoting the phosphorylation of AKT signaling. Due to its ability to promote the overgrowth of esophageal cancer cell, miR-502 may be a novel target for esophageal cancer therapeutic.

Keywords: AKT; ERK; Esophageal cancer; MicroRNA; TE-1; miR-502.