Fig. 6From: NOX4-derived ROS-induced overexpression of FOXM1 regulates aerobic glycolysis in glioblastomaAltered NOX4-FOXM1 signaling modulates tumorigenesis in vivo. A H&E staining of the sections of xenograft mouse brains. Scale bar, 1 mm. B Tumor size (mm3) was measured. C-D IHC and Western blot analysis of the indicated proteins in tumor tissue samples from the indicated groups. Scale bar, 20 μm. E Cellular ATP levels were determined in tumors from xenograft mice. F Schematic model of NOX4-FOXM1 signaling-regulated aerobic glycolysis and progression in glioblastoma cells. In glioblastoma cells, NOX4-generated mitochondrial ROS mediate HIF-1α stabilization. Stabilized HIF-1α can directly bind to the FOXM1 promoter and subsequently promote the expression of FOXM1, resulting in aerobic glycolysis and progression. *, P < 0.05; **, P < 0.01; ***, P < 0.001Back to article page