LINC00261 Inhibits Esophageal Cancer Radioresistance By Downregulating microRNA-552-3p And Promoting DIRAS1

Abstract

Background: Esophageal cancer (EC) is a life-threatening tumor with a high increasing incidence rate. Long intergenic non-protein coding RNAs (LINCs) are widely researched in EC. This study set out to investigate the role of LINC00261 in EC radioresistance.Methods: Radioresistant EC cell lines TE-1-R and TE-5-R were established using TE-1 and TE-5 cells. LINC00261, microRNA (miR)-552-3p, and DIRAS1 expression in EC tissues and adjacent normal tissues and EC cells was evaluated. Then, survival fraction (SF), colony formation, apoptosis, and γ-H2AX expression were analyzed. The binding relation between LINC00261 and miR-552-3p and between miR-552-3p and DIRAS1 were detected. Eventually, xenograft transplantation was applied to confirm the effect of LINC00261 on EC radioresistance in vivo.Results: LINC00261 and DIRAS1 were weakly expressed in EC tissues and cells, but miR-552-3p was overexpressed. For EC cells with X-ray radiation, overexpression of LINC00261 reduced SF and cell viability, strengthened γ-H2AX expression, and promoted apoptosis, which were all counteracted by miR-522-3p overexpression or DIRAS1 silencing. Mechanically, the binding relation between LINC00261 and miR-552-3p and between miR-552-3p and DIRAS1 were verified. In addition, LINC00261 overexpression suppressed tumor growth and reduced EC radioresistance in vivo.Conclusion: LINC00261 could suppress EC radioresistance via the competing endogenous RNA network to sponge miR-552-3p and upregulate DIRAS1 transcription.