Fig. 6

Sim enhanced the sensitivity of Sora by down-regulating the HIF-1α/PKM2 axis. (a) FG-4592, the activator of HIF-1α, and BAY87–2243, the inhibitor of HIF-1α were used to explore the role of HIF-1α on PPAR-γ and PKM2 by western blotting. (b) The analysis of nuclear expression of HIF-1α, PPAR-γ and PKM2 after treated with BAY87–2243 or FG-4592. (c) Rosiglitazone, the activator of PPAR-γ, and GW9662, the inhibitor of PPAR-γ were used to explore the role of PPAR-γ on HIF-1α and PKM2 by western blotting. (d) The analysis of nuclear expression of HIF-1α, PPAR-γ and PKM2 after treated with Rosiglitazone or GW9662. (e) Compound 3 k, the inhibitor of PKM2, and DASA 58, the activator of PKM2 were used to explore the role of PKM2 on HIF-1α and PPAR-γ by western blotting. (f) The analysis of nuclear expression of HIF-1α, PPAR-γ and PKM2 after treated with compound 3 k or DASA 58. (g) Verification of PKM2 over expression in LM3 cells via lentivirus transfection. (h) The verification of PKM2 knockdown in LM3-SR cells via lentivirus transfection. (i) Western blotting analysis of critical proteins in LM3 cells over expressing PKM2 or in LM3-SR cells with PKM2 knocked-down. (j) Glycolysis levels in LM3 cells over expressing PKM2 or in LM3-SR cells with PKM2 knocked-down. Results indicated by lactate production and glucose uptake levels. (k) CCK8 analysis of the effect of Sora in LM3-PKM2-OE cells at 24 h, 48 h and 72 h. (l) Effect of Sora and Sora + Sim co-treatment on LM3-SR-PKM2-KD cells. The data were represented as mean ± SD. * indicates p < 0.05 vs. CTRL or EV group