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. 2014 Aug 27;289(43):29739–29749. doi: 10.1074/jbc.M114.584821

FIGURE 5.

FIGURE 5.

PDK4 potentiates HIF-1α and its target PKM2 and promotes aerobic glycolysis. a, cell lysates from NIH/3T3 transfected with PDK4 expression plasmids or control plasmids and PC3 with shScr or shPDK4 were collected and analyzed by immunoblotting. b and c, glucose consumption (b) and lactate production (c) of control or PDK4-overexpressing NIH/3T3 cells treated with or without 10 nm rapamycin (R) for 48 h. d, immunoblotting of indicated proteins in control and PDK4 knockdown human cancer cells (PC3, A549, and MCF7). Glucose consumption (e) and lactate production (f) in control or PDK4-knockdown human cancer cells (n = 3) are shown. g, glucose consumption and lactate production of shScr or shPDK4 NIH/3T3 cells transfected with siRNA for PDH or negative control siRNA treated with or without 10 nm rapamycin for 48 h. Data are presented as the mean ± S.E. nc indicates negative control. V indicates control plasmids. *, p < 0.05. **, p < 0.01; ***, p < 0.001. RU indicates relative units.