LINC01711 通过作为 miR-34a 的竞争性内源性 RNA 并促进 ZEB1 表达，促进转化生长因子-β（TGF-β）诱导的多形性胶质母细胞瘤（GBM）侵袭。
LINC01711 promotes transforming growth factor-beta (TGF-β) induced invasion in glioblastoma multiforme (GBM) by acting as a competing endogenous RNA for miR-34a and promoting ZEB1 expression.
机构信息
Department of Biological Sciences, Birla Institute of Technology and Science, Pilani, Hyderabad Campus, Jawahar Nagar, Hyderabad 500 078, Telangana, India.
Department of Biological Sciences, Birla Institute of Technology and Science, Pilani, Hyderabad Campus, Jawahar Nagar, Hyderabad 500 078, Telangana, India.
出版信息
Neurosci Lett. 2023 Jan 1;792:136937. doi: 10.1016/j.neulet.2022.136937. Epub 2022 Oct 27.
GBM is the central nervous system's most aggressive and malignant tumor. TGF-β expression is elevated in GBM, and it promotes invasion and EMT. TGF-β regulates the expression of several lncRNAs, which promote glioma pathogenesis. Here we characterize the role of TGF-β-induced lncRNA- LINC01711 in glioma pathogenesis. We show that LINC01711 expression is significantly upregulated in GBM tissues and is associated with poor overall survival of GBM patients. Loss-of-function studies illustrate that LINC01711 promotes proliferation, migration, and invasion in GBM. In addition, LINC01711 depletion sensitizes glioma cells to Temozolomide (TMZ) induced apoptosis by inhibiting ZEB1 expression. LINC01711 functions as a competing endogenous RNA for miR-34a and promotes ZEB1 expression to regulate invasion. Our findings suggest that LINC01711 is an attractive therapeutic target for GBM.
GBM 是中枢神经系统中侵袭性最强和恶性程度最高的肿瘤。TGF-β在 GBM 中表达上调，并促进侵袭和 EMT。TGF-β调节几种 lncRNA 的表达，这些 lncRNA 促进神经胶质瘤的发病机制。在这里，我们描述了 TGF-β诱导的 lncRNA-LINC01711 在神经胶质瘤发病机制中的作用。我们发现 LINC01711 在 GBM 组织中表达显著上调，并与 GBM 患者的总生存期不良相关。功能丧失研究表明，LINC01711 促进 GBM 中的增殖、迁移和侵袭。此外，LINC01711 耗竭通过抑制 ZEB1 表达使神经胶质瘤细胞对替莫唑胺（TMZ）诱导的细胞凋亡敏感。LINC01711 作为 miR-34a 的竞争性内源性 RNA 发挥作用，促进 ZEB1 表达以调节侵袭。我们的研究结果表明，LINC01711 是 GBM 有吸引力的治疗靶点。
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