Long Non-Coding RNA LINC02532 Mediates p-AKT to Regulate Gastric Cancer Cell Activities Through Targeting miR-362-5p

Abstract

LINC02532 and miR-362-5p modulates gastric cancer (GC) cell activities. Herein, we elucidated the role of LINC02532 targeting miR-362-5p to mediate p-AKT in GC cells, aiming to provide a theoretical basis for clinical treatment. Human GC cells were treated with si-LINC02532, si-NC, LINC02532+miR-362-5p inhibitor and p-AKT inhibitor. LINC02532 and miR-362-5p expression was determined by RT-qPCR and p-AKT expression was detected. Transwell assay assessed cell invasion and migration upon treatment and the targeting relationship of LINC02532 and miR-362-5p was evaluated. A positive expression of LINC02532 and miR-362-5p was detected in each group of GC cells. The expression of LINC02532 was up-regulated (2.95 ± 0.23) and miR-362-5p was down-regulated (0.35 ± 0.08). Silence of LINC02532 significantly suppressed GC cell behaviors and inhibited migration speed of cancer cells, while p-AKT inhibitor treatment resulted in a decrease in the number of invaded and migrated cells. Combination of LINC02532 and miR-362-5p inhibitor was not effective as previous two treatments, but still decreased cell migration and invasion (p < 0.05). The luciferase experiment indicated LINC02532 targeted miR-362-5p. Down-regulation of LINC02532 also reduced p-AKT protein expression. p-AKT inhibitor group had a lower level of p-AKT protein, followed by LINC02532+miR-362-5p inhibitor group, and si-NC group. In conclusion, silence of LINC02532 reduces miR-362-5p and p-AKT protein expression in GC cells to suppress GC cell growth through inhibition of p-AKT signaling pathway.