Long Intergenic Non-Protein-Coding RNA 01138 Accelerates Tumor Growth and Invasion in Gastric Cancer by Regulating miR-1273e.

BACKGROUND The treatment and nursing of gastric cancer (GC) remains an enormous challenge in clinical practice. Understanding the potential mechanisms of the pathogenesis of GC would improve GC therapy. Long intergenic non-protein-coding RNA 01138 (LINC01138) was reported to promote the progression of hepatocellular carcinoma; however, whether it is involved in GC progression has been unclear. MATERIAL AND METHODS Expressions of LINC01138 and miR-1273e in GC tissues and cell lines were measured by qRT-PCR assay. The interaction between LINC01138 and miR-1273e was predicted by the online tool miRDB, verified by dual-luciferase reporter and RNA pulldown assays. Effects of LINC01138 knockdown or miR-1273e overexpression on cell viability, proliferation, apoptosis, invasion, and migration were evaluated by MTT, colony formation assay, flow cytometry, and Transwell assays. Target genes of miR-1273e were predicted by KEGG analysis, and involvement of the mitogen-activated protein kinase (MAPK) pathway was confirmed by qRT-PCR assay. RESULTS LINC01138 was increased but miR-1273e was decreased in GC tissues and cell lines. Knockdown of LINC01138 suppressed GC cell viability, proliferation, invasion, and migration, and promoted GC cell apoptosis. We demonstrated that LINC01138 contributed to GC progression by directly sponging and inhibiting miR-1273e. Moreover, the MAPK pathway was verified to participate in the promotive effects of LINC01138 on GC progression. CONCLUSIONS LINC01138 activated the MAPK signaling pathway by inhibiting miR-1273e to promote GC cell proliferation, invasion, and migration, and inhibit GC cell apoptosis, suggesting that the LINC01138/miR-1273e/MAPK axis is a promising therapeutic target for GC.