ROS promoted HIF-1α and VEGF expression in subclone cells.

<p>A, ROS led to increased expression of HIF-1α and VEGF in SKBR3 subclones. SKBR3 subclones showed higher normoxic and hypoxic HIF-1α level than the parental SKBR3 cells. VEGF expression was more increased in SKBR3 subclones than in the parental SKBR3 cells. HIF-1α and VEGF expression in SKBR3 subclone were significantly inhibited by NAC. B, ROS led to increased expression of HIF-1α and VEGF in 4T1 subcloneswhereas NAC was able to attenuate the ROS induced expression of HIF-1α and VEGF. C–D, H₂O₂ promoted HIF-1α expression, while PEG-catalase and mito-TEMPO inhibited HIF-1α expression in A clone (C) and C clone (D).