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

GBM is the central nervous system's most aggressive and malignant tumor. TGF-beta expression is elevated in GBM, and it promotes invasion and EMT. TGF-beta regulates the expression of several lncRNAs, which promote glioma pathogenesis. Here we characterize the role of TGF-beta-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.

Automated summary

GBM is an aggressive and malignant tumor in the central nervous system. TGF-beta expression is elevated in GBM and promotes invasion and EMT. Several lncRNAs regulated by TGF-beta promote glioma pathogenesis, including LINC01711. LINC01711 is significantly upregulated in GBM tissues and associated with poor overall survival in patients, and it promotes proliferation, migration, and invasion in GBM. Depletion of LINC01711 sensitizes glioma cells to TMZ-induced apoptosis by inhibiting ZEB1 expression, and it functions as a competing endogenous RNA for miR-34a to promote ZEB1 expression and regulate invasion. LINC01711 appears to be a promising therapeutic target for GBM.