Collectively, these results indicate that AMP-induced growth inhibition and apoptosis in breast cancer cells are partially dependent on ER stress through up-regulation of CHOP expression via activating two branches of unfolded protein response (UPR), PERK and ATF6, and that PERK-CHOP pathway may be mainly involved in ER stress-mediated apoptosis induced by AMP. This evidence concerns the gene DDIT3 and breast cancer.