Propyl gallate reduces the growth of lung cancer cells through caspase‑dependent apoptosis and G1phase arrest of the cell cycle.

Abstract

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 800µM at24h based on MTT assays. DNA flow cytometry showed that PG induced G1phase 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 AnnexinV‑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; ∆Ψm) and decreased MMP (∆Ψm) 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 G1phase arrest of the cell cycle.