Glioma is characterized by high morbidity, high mortality and poor prognosis. Recent studies exhibited that lncRNA CCAT2 is overexpressed in glioma and promotes glioma progression, but the specific molecular biological mechanism remains to be determined. We performed qRT-PCR to evaluate the expression of related genes, Western blotting analysis to measure protein levels, colony formation assay to detect the proliferative ability of glioma cells, flow cytometry to measure cell apoptosis, bioinformatics analysis and dual luciferase assay to verify the binding sites and the targeted regulatory relationship in A172 and U251 cell lines and tube formation assay to determine endothelial angiogenesis. LncRNA CCAT2 and VEGFA were highly expressed, while miR-424 was expressed at low levels in NHA cells. Furthermore, knockdown of lncRNA CCAT2 decreased cell proliferation, increased cell apoptosis and inhibited endothelial angiogenesis in glioma. Moreover, lncRNA CCAT2 shared a complementary sequence with miR-424 which in turn directly bound to the 3'-UTR of VEGFA. Further investigation indicated that lncRNA CCAT2 promoted cell proliferation and endothelial angiogenesis by inducing the PI3K/AKT signalling pathway in glioma. The oncogenic lncRNA CCAT2 is highly associated with the development of glioma and exerts its function by upregulating VEGFA via miR-424.
Keywords: Angiogenesis; Glioma; VEGFA; lncRNA CCAT2; miR-424.