Skip to main content
Fig. 6 | Molecular Medicine

Fig. 6

From: Ginsenoside Rh2 shifts tumor metabolism from aerobic glycolysis to oxidative phosphorylation through regulating the HIF1-α/PDK4 axis in non-small cell lung cancer

Fig. 6

G-Rh2 targeted inhibition of PDK4 expression promoted mitochondrial oxidative phosphorylation. (A) Western blot detection of PDK4 protein expression following G-Rh2 and DCA treatment. (B) Molecular docking modeling predicts the binding of G-Rh2 to PDK4. (C) ATP production in A549 cells after G-Rh2 and DCA treatment. (D) Glucose intake in A549 cells after G-Rh2 and DCA treatment. (E) Lactification in A549 cells after G-Rh2 and DCA treatment. (F) Pyruvic acid production in A549 cells after G-Rh2 and DCA treatment. (G) PDH activity in A549 cells after G-Rh2 and DCA treatment. (H-J) Fluorescence detection and flow cytometry analysis of ROS levels in A549 cells after G-Rh2 and DCA treatment. Data are expressed as mean ± SD. (K, L) ECAR measured with Seahorse XF in A549 cells and A549 cells treated with G-Rh2 and DCA. 2-DG, 2-deoxyglucose. (M, N) OCR measured with Seahorse XF in A549 cells and A549 cells treated with G-Rh2 and DCA. FCCP, carbonyl cyanide 4-(trifluoromethoxy) phenylhydrazone. (O, P) ECAR measured with Seahorse XF in A549 and PDK4 overexpressing A549 cells treated with G-Rh2. (Q, R) OCR measured with Seahorse XF in A549 cells and PDK4 overexpressing A549 cells treated with G-Rh2. **P < 0.01, ***P < 0.001, ****P < 0.001 vs. the control group

Back to article page

Molecular Medicine

ISSN: 1528-3658