Fig. 4

Leptin increased PKM2 expression and induced EMT in breast cancer cells via the activation of PI3K/AKT. a Serum-starved MCF-7 and SK-BR-3 cells were treated with PD98059 (MAPK inhibitor, 1.34 μmol/mL), AG490 (STAT3 inhibitor, 5 μmol/mL) and LY294002 (PI3K inhibitor, 10 μmol/mL) for 1 h, followed by 200 ng/mL leptin treatment for 24 h. DMSO was used as a control. Western blotting analysis demonstrated that the PI3K inhibitor LY294002 abolished leptin-mediated increase in PKM2 expression in MCF-7 and SK-BR-3 cells (P < 0.05). b Antibodies against ObR (4 μg/mL) abolished the leptin-mediated increase in p-AKT, p-PKM2 and PKM2 expression in MCF-7 and SK-BR-3 cells (P < 0.05). c The PI3K inhibitor LY294002 abolished leptin-mediated downregulation of E-cadherin expression and the upregulation of vimentin, fibronectin, p-PKM2 and PKM2 expression in MCF-7 and SK-BR-3 cells