Long Noncoding RNA LINC00265 Promotes Proliferation of Gastric Cancer by Acting as A Competing Endogenous RNA on microRNA-144-3p Thereby Upregulating CBX4

Abstract

Background:The expression levels and detailed functions of LINC00265 in gastric cancer (GC) have not yet been explored. This study aimed to measure LINC00265 expression in GC tissues and cell lines, investigate its specific roles in the aggressive characteristics of GC cells in vitro and in vivo, and elucidate the regulatory mechanisms of LINC00265 action.Materials and methods: The qRT-PCR was performed to test the RNA expression levels in GC tissues and cell lines. Cell proliferation was detected by CCK-8 and colony formation assays. Western blot assay was used to measure relevant protein expression. Luciferase reporter assays were performed to investigate the association between LINC00265 and microRNA-144-3p and CBX4.Results: LINC00265 expression was high in GC tissue samples and cell lines; LINC00265 overexpression correlated with shorter overall survival of the patients. A LINC00265 knockdown inhibited GC cell proliferation in vitro and slowed tumor growth in vivo. Mechanism investigation revealed that LINC00265 acts as a competing endogenous RNA on microRNA-144-3p (miR- 144) in GC cells. Chromobox 4 (CBX4) mRNA was identified as a direct target of miR-144-3p in GC cells. The knockdown of miR-144-3p counteracted the reduction in the malignant characteristics of GC cells by the downregulation of LINC00265.Conclusion: In conclusion, LINC00265 functions as a competing endogenous RNA targeting miR-144-3p and increases the malignancy of GC cells in vitro and in vivo by upregulating CBX4.