Fig. 5
From: Cardamonin inhibits breast cancer growth by repressing HIF-1α-dependent metabolic reprogramming
Restoring the HIF-1α/PDHK1 pathway abolishes the effect of cardamonin on mitochondrial oxidative phosphorylation and cell viability in MDA-MB-231 cells. a CoCl2 (100 μM) pre-stimulation for 6 h restored protein expression of HIF-1α and PDHK1 in cardamonin treated cells. b, c CoCl2 (100 μM) pre-treatment suppressed the cardamonin-induced OCR upregulation in MDA-MB-231 cells. d CoCl2 (100 μM) pre-treatment restored cell viability in cardamonin-treated MDA-MB-231 cells. e CoCl2 (100 μM) pre-treatment reversed the ROS accumulation in cardamonin-treated MDA-MB-231 cells. f NAC (N-acetyl-cysteine, ROS scavenger; 5 mM) pretreatment abolished the inhibitory effect of cardamonin (20 μM) on cell viability in MDA-MB-231 cells. g PDHK1 expression construct (GV230-PDHK1) was introduced in MDA-MB-231 cells by transiently transfection, and protein expression was assessed by western blot. h PDHK1 overexpression rescued cell viability in cardamonin-treated MDA-MB-231 cells. Data are shown as mean ± SD; *, P < 0.05, **, P < 0.01; ***, P < 0.001, ns means no statistical difference, compared with control. n ≥ 3