LINC00473 has been reported to be aberrantly expressed in diverse kinds of human malignancy. However, the function and underlying mechanisms of LINC00473 in glioma still remain unclear. In the present study, LINC00473 was notably elevated in glioma tissues and cell lines. High LINC00473 expression was associated with advanced WHO grade (III-IV), low Karnofsky performance score (KPS), and poor prognosis. Loss function assays showed that LINC00473 knockdown decreased glioma cell proliferation, invasion and epithelial-mesenchymal transition (EMT) processes in vitro, and reduced tumor growth in vivo. Mechanistic analysis indicated that LINC00473 regulated CDK6 expression by competitively binding to miR-637. Moreover, rescue assays revealed that miR-637 inhibitors abolished the effects of LINC00473 suppression on glioma cells progression. Thus, we demonstrated that LINC00473 could act as a ceRNA of miR-637 to promote glioma progression through regulating CDK6 expression, which provided a potential therapeutic target for treatment of glioma patients.

中文翻译：

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长的非编码RNA LINC00473通过损害miR-637 / CDK6轴来促进神经胶质瘤细胞的增殖和侵袭。

据报道，LINC00473在多种人类恶性肿瘤中异常表达。但是，LINC00473在神经胶质瘤中的功能和潜在机制仍不清楚。在本研究中，LINC00473在神经胶质瘤组织和细胞系中显着升高。LINC00473高表达与WHO分级高（III-IV），Karnofsky评分低（KPS）和预后差有关。损失功能分析表明，LINC00473敲低可降低神经胶质瘤细胞的增殖，体外侵袭和上皮-间充质转化（EMT）过程，并减少体内肿瘤的生长。机理分析表明，LINC00473通过竞争性结合miR-637调节CDK6表达。此外，急救试验表明，miR-637抑制剂消除了LINC00473抑制对神经胶质瘤细胞进展的影响。从而，