Fig. 5
G-Rh2 inhibited tumor aerobic glycolysis by regulating HIF1-α/PDK4. (A-B) Volcano plots showing 176 upregulated and 586 downregulated differentially expressed proteins in A549 cells after G-Rh2 treatment compared to the control group,. (C) COG analysis histogram after G-Rh2 treatment, compared to the control group. (D) Clustered heat map showing a portion of A549 cells after G-Rh2 treatment, compared to the control group. (E) KEGG pathway enrichment of proteomics in A549 cells. (F) Subcellular location analysis after G-Rh2 treatment, compared to the control group. (G) GO pathway enrichment of proteomics in A549 cells. (H) Molecular docking modeling predicting the binding of G-Rh2 to HIF-1α. (I) Western blot detection of PDK4 protein expression. (J)Western blot detection of HIF1-α and VEGF protein expression. (K) RT-qPCR detection of downstream genes of HIF1-α. (L) Glucose intake in A549 cells after G-Rh2 treatment. (M) Lactification in A549 cells after G-Rh2 treatment. (N) Western blot detection of glycolytic protein expression. (O, P) PET-CT detection of the concentration of 18FDG in A549 tumors, revealing glucose intake after G-Rh2 treatment in xenografts of nude mice. (Q) γ-count data showing glucose intake of A549 tumors after G-Rh2 treatment in xenografts of nude mice. Data are expressed as mean ± SD.**P < 0.01, ***P < 0.001, ****P < 0.001 vs. the control group