Fig. 2
From: PKM2 is the target of proanthocyanidin B2 during the inhibition of hepatocellular carcinoma
PB2 inhibited the aerobic glycolysis level in HCC cells. a The effects of PB2 on glucose uptake and lactate concentration in five HCC cell lines and L02 cells. b Western blotting analysis of three rate-limiting enzymes and OXPHOS. PB2 treatment decreased the expression of HK2, PFKFB3, and PKM2, while it increased OXPHOS expression in a dose-dependent manner. c The qPCR analysis of 16 aerobic glycolysis-related genes. PKM2, HIF-1α, and HSP90 were the most changed genes after PB2 treatment. d A PKM2 agonist (DASA-58, 40 μM) was used to determine the role and location of PKM2 during the HCC inhibition effect of PB2 by western blotting. PB2 inhibited the expression of PKM2 in the nucleus. e The immunofluorescence staining of PKM2 in HCC cells (original magnification, 400×). PKM2 was detectable in both the cytoplasm and nucleus in the NC group, while PB2 not only suppressed the expression but also the nuclear localization of PKM2. *P < 0.05 vs. the NC group (2C: one-way ANOVA)