Angiogenesis is one of the critical biological elements affecting the development and progression of
cancer. Long non-coding RNAs (lncRNAs) are important regulators and aberrantly expressed in various types of human
cancer. Our previous studies indicated that
lncRNA taurine upregulated 1 (TUG1) implicated in the regulation of blood-
tumor barrier permeability; however, its role in
glioblastoma angiogenesis still unclear. Here we demonstrated that TUG1 was up-expressed in human
glioblastoma tissues and
glioblastoma cell lines. Knockdown of TUG1 remarkably suppressed
tumor-induced endothelial cell proliferation, migration and tube formation as well as reducing spheroid-based angiogenesis ability in vitro, which are the critical steps for
tumor angiogenesis. Besides, knockdown of TUG1 significantly increased the expression of mircroRNA-299 (miR-299), which was down-expressed in
glioblastoma tissues and
glioblastoma cell lines. Bioinformatics analysis and
luciferase reporter assay revealed that TUG1 influenced
tumor angiogenesis via directly binding to the miR-299 and there was a reciprocal repression between TUG1 and miR-299 in the same
RNA-induced silencing complex. Moreover, knockdown of TUG1 reduced the expression of
vascular endothelial growth factor A (VEGFA), which was defined as a functional downstream target of miR-299. In addition, knockdown of TUG1, shown in the in vivo studies, has effects on suppressing
tumor growth, reducing
tumor microvessel density and decreasing the VEGFA expression by upregulating miR-299 in xenograft
glioblastoma model. Overall, the results demonstrated that TUG1 enhances
tumor-induced angiogenesis and
VEGF expression through inhibiting miR-299. Also, the inhibition of TUG1 could provide a novel therapeutic target for
glioblastoma treatment.