The addition of Z-VAD-FMK, a cell-permeable pan-caspase inhibitor, blocked the cleavage of both PARP and Caspase 3, which further confirmed that CPX induced apoptosis in NSCLC cells (Additional file 1: Fig. S4).Together, these findings reveal that CPX inhibits the growth of NSCLC cells, at least in part, by way of activation of PERK-dependent ER stress and UPRER to induce apoptosis. This evidence concerns the gene CASP3 and non-small cell lung carcinoma.