MiR-221 affects proliferation and apoptosis of gastric cancer cells through targeting SOCS3.

Abstract

The suppressors of cytokine signaling 3 (SOCS3) negatively regulates the JAK-STAT pathway. The bioinformatics analysis revealed a targeted binding site between miR-221 and the 3'-UTR of SOCS3 mRNA. This study investigated the role of miR-221 in the proliferation and apoptosis of gastric cancer cells. The Dual-Luciferase reporter gene assay validated the target relationship between miR-221 and SOCS3. Gastric cancer tissues were collected and compared with adjacent tissues to detect the expression of miR-221 and SOCS3. The Kaplan-Meier method was used to analyze the survival rate between patients with high and low miR-221 expression. Human gastric cancer SGC7901 cells were cultured and divided into the miR-NC group and miR-221 inhibitor group, followed by an analysis of the expression of miR-221, SOCS3, p-JAK2 and p-STAT3, cell apoptosis, and proliferation. Compared with adjacent tissues, miR-221 expression was significantly increased in tumor tissues, and SCOS3 mRNA expression was decreased. Compared with those with lower miR-221 expression, the prognosis of patients with higher miR-221 expression was significantly worse. There was a targeted regulatory relationship between miR-221 and SOCS3 mRNA. Compared with GES-1 cells, miR-221 expression in gastric cancer MGC803 and SGC7901 was significantly increased, and the expression of SOCS3 mRNA and protein was significantly decreased. The transfection of miR-221 inhibitor significantly increased SOCS3 expression in gastric cancer SGC7901 cells, decreased p-JAK2, p-STAT3 protein expression, increased cell apoptosis, and decreased cell proliferation. Increased miR-221 expression and decreased SOCS3 expression are related to gastric cancer. MiR-221 regulates the proliferation and apoptosis of gastric cancer cells by regulating SOCS3 expression.