Increasing findings are suggesting the vital roles of long noncoding RNAs (lncRNAs) in the glioblastoma tumorigenesis. However, whether the novel lncRNA LINC00021 modulates temozolomide (TMZ) resistance of glioblastoma is still unclear. Clinically, lncRNA LINC00021 was significantly up‐regulated in glioblastoma, especially the TMZ‐resistant tissue and cells, and the LINC00021 overexpression was closely correlated to TMZ resistance and unfavorable prognosis. Functionally, LINC00021 positively promoted the TMZ resistance and reduced apoptosis. Mechanistically, transcription factor E2F1 activated the expression of LINC00021. Moreover, LINC00021 regulated the glioblastoma TMZ resistance through Notch pathway and epigenetically silenced p21 expression via recruiting EZH2. Collectively, present research indicates the critical roles of lncRNA LINC00021 in glioblastoma genesis, providing a novel insight for TMZ resistance in glioblastoma.

中文翻译：

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长基因间非编码 RNA 00021 通过 Notch 通路表观遗传沉默 p21 促进胶质母细胞瘤替莫唑胺耐药

越来越多的研究结果表明，长链非编码 RNA (lncRNA) 在胶质母细胞瘤发生中发挥着重要作用。然而，新型lncRNA LINC00021是否调节胶质母细胞瘤对替莫唑胺（TMZ）的耐药性尚不清楚。临床上，lncRNA LINC00021在胶质母细胞瘤中显着上调，尤其是在TMZ耐药的组织和细胞中，LINC00021的过表达与TMZ耐药和不良预后密切相关。在功能上，LINC00021 积极促进 TMZ 抗性并减少细胞凋亡。从机制上讲，转录因子 E2F1 激活了 LINC00021 的表达。此外，LINC00021 通过 Notch 通路调节胶质母细胞瘤 TMZ 抗性，并通过募集 EZH2 表观遗传沉默 p21 表达。总的来说，