Propyl gallate reduces the growth of lung cancer cells through caspase-dependent apoptosis and G1 phase arrest of the cell cycle

Propyl gallate (3,4,5-trihydroxybenzoic acid propyl ester; PG) is a synthetic phenolic antioxidant which exerts many effects on tissue and cell functions. In the present study, Calu-6 and A549 lung cancer cells were used to examine the molecular mechanism of the anti-growth effects of PG in relation to apoptosis and cell cycle arrest. PG inhibited the growth of both lung cancer cell types in a dose-dependent manner with an IC50 of 800 mu M at 24 h based on MTT assays. DNA flow cytometry showed that PG induced G1 phase arrest of the cell cycle in Calu-6 and A549 cells. In addition, PG induced apoptosis in both lung cancer cell types, as evidenced by sub-G1 cell population and Annexin V-stained cells. Western blot results demonstrated that PG decreased the Bcl-2 level which was accompanied by an increase in the cleaved form of poly(ADP-ribose) polymerase (PARP). PG also triggered loss of mitochondrial membrane potential (MMP; increment psi m) and decreased MMP ( increment psi m) levels in both lung cancer cell types, as assessed by FACS analysis. Furthermore, PG upregulated the activities of caspase-3 and caspase-8 in Calu-6 cells. In conclusion, PG treatment inhibited the growth of lung cancer cells, especially Calu-6 cells via caspase-dependent apoptosis as well as G1 phase arrest of the cell cycle.