Fig. 5.

ENO1 and PKM promote HCC progression and HBV replication by modulating glycolysis. (A-B) According to glycolysis assay, PKM silencing suppressed glucose consumption (A) and lactate production (B) of HepG2.2.15 cells, whereas this influence was reversed by ENO1 overexpression. (C-E) Analysis of metabolic intermediates implied the inhibition of PKM silencing on the production of pyruvate (C), G6PD (D), and 2-PG (E) of HepG2.2.15 cells. ENO1 overexpression counteracted this effect of PKM silencing. (F) PKM silencing in HepG2.2.15 cells decreased NADPH/NADP+ ratio, which was reversed by ENO1 overexpression. (G) qRT-PCR indicated that the inhibition of PKM silencing on HBV DNA replication in HepG2.2.15 cells was abrogated by ENO1 overexpression. (H) According to ELISA, PKM silencing reduced HBsAg level in HepG2.2.15 cells, but ENO1 overexpression eliminated this effect. (I) Western blot implied that, the repression of PKM silencing on HBx protein expression was counteracted by ENO1 overexpression. *** P < 0.001 vs. the Control group. ## P < 0.01 vs. the ENO1 group. ^^ P < 0.01 vs. the siPKM group