Fig. 7

SOX9 is a downstream target of telmisartan. A The red and green bars represent the top ten most upregulated and downregulated genes, respectively. B left, Kaplan‒Meier overall survival and B middle, disease-free survival analyses revealed that the overexpression of SOX9 was associated with poor prognosis in glioma patients from the TCGA dataset. B right, SOX9 is overexpressed in LGG and GBM compared with normal controls. C Western blots showing levels of SOX9 induced by telmisartan in glioma cells. β-Actin was used as a loading control. D Glioma cells were transfected with the full-length human SOX9 plasmid. The overexpression of SOX9 was confirmed by western blotting. pcDNA3.1 was used as a transfection control. The quantification of abovementioned proteins relative to GAPDH was revealed in the right (n = 3). *p < 0.05. E Comparative MTS assay demonstrating the effect of SOX9 overexpression on LN229, U87MG, and LNZ308 cells treated with telmisartan at 48 h. Values are expressed relative to the control group (n = 3, error bars indicate ± SD). HR, hazard ratio; N, normal control; p(HR), pooled hazard ratio; T, tumor; TPM, transcripts per million; LGG, low-grade glioma. *p < 0.01. These data demonstrate SOX9 is a downstream target of telmisartan because SOX9 expression in glioma cells were dose-dependently inhibited by telmisartan. Moreover, GBM cells with Sox9 overexpression had a higher cell viability rate than control cells