Fig. 1

Phosphorylation of AMPK was suppressed by Kras mutation in CRC cells. a MTS analysis of DLD1 WT (+/−) and Kras mutation (G13D/−) cells treated with cetuximab (Cet) at the indicated doses for 48 h. b Apoptosis in DLD1 WT (+/−) and Kras mutation (G13D/−) cells treated with 5 nM Cet for 48 h was analyzed by nuclear staining with Hoechst 33258. c Apoptosis in DLD1 WT (+/−) and Kras mutation (G13D/−) cells treated with 5 nM Cet for 48 h was analyzed by Annexin V staining followed by flow cytometry. d Western blot of p-AMPK, AMPK, and Caspase-3 (C3) in the cells treated as in (b). e DLD1 WT (+/−) cells stably expressing control, Kras WT, or Kras mutant (G12V) by retrovirus transfection were treated with Cet at indicated doses for 48 h. The cell viability was analyzed by MTS assay. f DLD1 WT (+/−) cells stably expressing control, Kras WT, or Kras mutant (G12V) by retrovirus transfection were treated with 5 nM Cet for 48 h. The expression of indicated proteins was analyzed western blot. g MTs analysis of indicated cells treated with Cet at indicated doses for 48 h. The IC50 was calculated and plotted in the right panel. h The expression of p-AMPK, AMPK in the indicated cells treated with 5 nM Cet. Each experiment was repeated for 3 times. *, p < 0.05; **, p < 0.01