The role and mechanisms of long non-coding RNA LINC00662 in promoting the proliferation, migration, and angiogenesis of BGC-823 and HGC-27 cells and the subsequent effect on the progression of gastric cancer.

Abstract

A large body of evidence indicates that long non-coding ribonucleic acid (lncRNA) is widely involved in various cellular processes and tumor progression. LINC00662, an lncRNA, has been reported to play a role in lung cancer. However, the biological function of LINC00662 in gastric cancer (GC) has not yet been explored. This study aimed to investigate the role and mechanisms of LINC00662 in promoting the proliferation, migration, and angiogenesis of BGC-823 and HGC-27 cells and the subsequent effect on the progression of GC. The expression level of LINC00662 in GC tissues and cells was detected by quantitative reverse transcription polymerase chain reaction. Small interfering RNA was used to silence LINC00662 in BGC-823 and HGC-27 GC cells in vitro for an MTT assay, a colony formation assay, and a transwell assay to determine cell proliferation and invasion ability. LINC00662-silenced BGC-823 and HGC-27 cells were also injected into zebrafish to detect the proliferation and invasion ability of the cells. Co-cultures in vitro of human umbilical vein endothelial cells (HUVECs) with silenced LINC00662 and in vivo experiments were also performed. The upregulation of LINC00662 was observed in GC tissues and cell lines. Functional studies in vitro showed that knocking down LINC00662 inhibited the proliferation and invasion of GC cells. In vivo experiments in zebrafish also confirmed that knocked-down LINC00662 inhibited the proliferation and invasion of GC cells, and in vitro angiogenesis experiments showed that the supernatant of GC with knocked-down LINC00662 inhibited the angiogenesis of HUVECs. LINC00662 promoted the proliferation, invasion, and migration of GC cells and promoted angiogenesis. These findings suggest that LINC00662 may be a potential therapeutic target for GC.