[Inhibition of autophagy initiation stage enhances camptothecin-induced apoptosis in NCI-H1975 cells].

Objective To explore the effect of autophagic inhibitors chloroquine (CQ) and 3-methyl adenine (3-MA) on apoptosis of non-small cell lung adenocarcinoma NCI-H1975 cells induced by camptothecin (CPT). Methods After NCI-H1975 cells were treated with CPT, cell proliferation was detected by CCK-8 assay, morphological changes of cells were observed by PI staining, and the apoptosis of NCI-H1975 cells was determined by flow cytometry. The levels of autophagy-and apoptosis-related proteins LC3I, LC3II, P62, caspase-3 and poly ADP-ribose polymerase (PARP) and transforming growth factor beta 1 (TGF-beta 1) were detected by Western blot analysis. Results After CPT treatment, the ratio of LC3II to LC3I was raised. The apoptotic protease caspase-3 and substrate PARP were obviously degraded, which could be enhanced by 3-MA but inhibited by CQ. It was also found that the intracellular TGF-beta 1 was reduced after CPT treatment. Conclusion Inhibition of autophagy initiation stage in NCI-H1975 cells can increase the sensitivity of cell apoptosis induced by CPT.