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.

中文翻译：

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LncRNA CCAT2通过激活miR-424来激活VEGFA信号，从而促进神经胶质瘤的血管生成。

胶质瘤的特征是高发病率，高死亡率和不良预后。最近的研究表明，lncRNA CCAT2在神经胶质瘤中过度表达并促进神经胶质瘤的进展，但具体的分子生物学机制尚待确定。我们进行了qRT-PCR以评估相关基因的表达，Western印迹分析以测量蛋白质水平，集落形成分析以检测神经胶质瘤细胞的增殖能力，流式细胞术以检测细胞凋亡，生物信息学分析和双重荧光素酶检测以验证结合位点和A172和U251细胞系中的靶向调节关系以及通过管形成测定来确定内皮血管生成。LncRNA CCAT2和VEGFA在NHA细胞中高表达，而miR-424在低水平表达。此外，抑制lncRNA CCAT2的表达可降低神经胶质瘤的细胞增殖，增加细胞凋亡并抑制内皮血管生成。此外，lncRNA CCAT2与miR-424共享互补序列，后者又直接与VEGFA的3'-UTR结合。进一步的研究表明，lncRNA CCAT2通过在神经胶质瘤中诱导PI3K / AKT信号通路来促进细胞增殖和内皮血管生成。致癌lncRNA CCAT2与神经胶质瘤的发生高度相关，并通过miR-424上调VEGFA发挥其功能。进一步的研究表明，lncRNA CCAT2通过在神经胶质瘤中诱导PI3K / AKT信号通路来促进细胞增殖和内皮血管生成。致癌lncRNA CCAT2与神经胶质瘤的发生高度相关，并通过miR-424上调VEGFA发挥其功能。进一步的研究表明，lncRNA CCAT2通过在神经胶质瘤中诱导PI3K / AKT信号通路来促进细胞增殖和内皮血管生成。致癌lncRNA CCAT2与神经胶质瘤的发生高度相关，并通过miR-424上调VEGFA发挥其功能。