Abstract
Background: Glioma is a kind of malignant brain tumor with high mortality. LncRNA is involved in the regulation of glioma development. The relationship between lncRNA and glioma progression needs further study. Whether LINC00160 is involved in the progression of glioma remains unclear. The purpose of this study was to investigate the role and mechanism of LINC00160 in glioma.
Methods: Tumor tissues were collected and human cell lines were purchased. RNA was extracted using Trizol reagent and analyzed through qRT-PCR. The survival rate was examined according to LINC00160 expression. siRNAs were used to knock down LINC00160 in tumor cells. miRDB and TargetScan were used to predict RNA interactions. RNA interaction was verified by luciferase reporter assay. Cell growth was evaluated using CCK8, colony formation, and transwell assay respectively. TCGA data was used to analyze RAB13 expression.
Results: The expression of LINC00160 was increased in glioma. High expression of LINC00160 was associated with poor prognosis. LINC00160 knockdown suppressed tumor proliferation, migration and invasion. LINC00160 sponges miR-629-3p to inhibit its binding to RAB13 mRNA, resulting in RAB13 upregulation. RAB13 overexpression reversed the inhibitory effects of LINC00160 knockdown on proliferation, migration and invasion.
Conclusion:Our findings support that LINC00160 exerts oncogenic roles in glioma progression through miR-629-3p/RAB13 axis.