Long Noncoding RNA TP53TG1 Contributes to Radioresistance of Glioma Cells Via miR-524-5p/RAB5A Axis.

Abstract

Background: Long noncoding RNAs (lncRNAs) have been reported to be important regulators in cancer. In this study, we aimed to discover the functions of lncRNA TP53TG1 in glioma. Methods: The expression of lncRNA TP53TG1, microRNA-524-5p (miR-524-5p) and RAB5A, a member RAS oncogene family (RAB5A), were examined by quantitative real-time polymerase chain reaction. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry were applied to analyze the proliferation and apoptosis of glioma cells. Colony formation assay was used to detect the colony formation ability and radioresistance of glioma cells. Western blot assay was performed to detect the expression of autophagy-associated proteins and RAB5A. StarBase software was utilized to predict the combination between miR-524-5p and TP53TG1 or RAB5A, and dual-luciferase reporter assay and RNA immunoprecipitation assay were used to verify the above predictions. Animal experiment using immunodeficient nude mice was conducted to detect the role of TP53TG1 in vivo. Results: Radiation stimulation (6 Gy) upregulated the abundance of TP53TG1. TP53TG1 potentiated radioresistance and progression of glioma by promoting the autophagy. miR-524-5p was verified as a direct downstream regulation of TP53TG1. miR-524-5p depletion attenuated the influence of TP53TG1 interference on the functions of glioma cells. RAB5A was a direct target of miR-524-5p as well. The inhibitory effect of miR-524-5p on the malignancy of glioma cells was overturned by overexpression of RAB5A. RAB5A was regulated by TP53TG1/miR-524-5p signaling in glioma cells. TP53TG1 silencing impeded the progression of glioma in vivo. Conclusion: lncRNA TP53TG1 accelerated the proliferation, colony formation, autophagy, and radioresistance, and restrained the apoptosis of glioma cells through miR-524-5p/RAB5A axis.