Fig. 4

De novo lipogenesis and octanoate mediate the activation of ABCB1 gene. A: Control or Ethidium Bromide treated (200ng/mL and 100ng/mL, respectively) CCRF-CEM and MOLT-4 cells were treated with the ACC1 inhibitor, ND-630, with the indicated concentration for 7 days and P-gp and β-actin accumulation visualized by immunoblotting. B: Control or Ethidium Bromide treated (200ng/mL and 100ng/mL, respectively, for 7 days) CCRF-CEM and MOLT-4 cells were treated with the indicated concentrations of octanoate for 24 h and the accumulation of P-gp and β-actin accumulation was visualized as above. C: Control CCRF-CEM and MOLT-4 cells were treated concomitantly with the indicated concentration of octanoate and the partial β-oxidation inhibitor, Ranolazine, and the accumulation of P-gp and β-actin accumulation was visualized as above. D: The scheme illustrates the following hypothesis: In cells with normal mitochondrial activity, DNL products and octanoate are degraded by the mitochondrial β-oxidation and therefore they would not be available to induce ABCB1 gene expression (left). In mitochondria-depleted cells, DNL products and octanoate are available and mediate the induction of ABCB1 gene