Toxic effects and reactive oxygen species generation were induced in lung cancer A549 cells. Alterations in the mitochondrion membrane potential and apoptotic morphological changes were recorded. Punicalagin also inhibited STAT-3 translocation and induced apoptosis by inhibiting expression of Bcl-2 and enhanced expression of Bax, cytochrome-c, caspase-9, and caspase-3 in A549 cells. Here, CASP3 is linked to lung carcinoma.