Long Non-Coding RNA LINC00202 Enhances Radiotherapy Sensitivity of Nasopharyngeal Carcinoma by Regulating Ras and Rab Interactor 1

Abstract

Radiotherapy resistance is a major problem faced in clinical treatment of nasopharyngeal carcinoma (NPC). This study aims to illustrate the role of LINC00202 in influencing radiotherapy resistance of NPC patients. Microarray analyses on differentially expressed long non-coding RNAs (lncRNAs) and their target miRNAs and mRNAs in the profiling containing radiotherapy resistant and sensitive NPC tissues were conducted. The biological functions of LINC00202 in regulating proliferative ability, cell cycle progression and apoptosis in irradiated HNE-2 cells were explored. In addition, in vivo effects of LINC00202 on NPC growth were examined by establishing the xenograft models. LINC00202 was downregulated in radiotherapy resistant NPC tissues and irradiation-induced radio resistant NPC cells. In vitro experiments showed that overexpression of LINC00202 in HNE-2 cells suppressed viability and induced cell cycle arrest in G1 phase. Survival rate of HNE-2 cells overexpressing LINC00202 dose-dependently decreased following different doses of irradiation. Consistently, 4-Gy irradiation in mice with in vivo expression of LINC00202 presented slower tumor growth of NPC than those of controls. Microarray analyses uncovered the LINC00202/miR-513A-5P/RIN1 axis, which was responsible for enhancing radiotherapy sensitivity of NPC. LINC00202/miR-513a-5p/RIN1 axis is responsible for enhancing radiotherapy sensitivity of NPC, which provides a new idea in clinical treatment of NPC.