Moreover, these treatments not only inhibited the expression of both c-MET and PARP-1 but also remarkably elevated the levels of autophagy markers (ATG-7, Beclin-1, and LC3-II) and the apoptotic markers (caspase-3 and Bax) with the inhibition of the P62 and Bcl-2 which collectively, boosts autophagy and apoptotic cell death of lung cancer cells. Here, BAX is linked to lung cancer.