The effect of eicosapentaenoic acid on the proliferation and apoptosis of gastric cancer cells

Abstract

Objective To observe the effect of eicosapentaenoic acid (EPA) on the proliferation and apoptosis of human gastric cancer cells and to explore the potential mechanism involved.Methods Human gastric cancer cell lines SGC-7901 and MGC-803 were treated with EPA at 10,20,40 μg/ml for 24-72 hours.The inhibition of cell proliferation was evaluated by methyl thiazolyl tetrazolium assay.The apoptosis and the distribution of cell cycle were analyzed by flow cytometry.Mitochondria membrane potential was determined with a fluorescence probe rhodamine 123.Cellular distribution of cytochrome C was quantitatively detected with enzyme-linked immunosorbent assay.Caspase-3 activity was measured with spectrofluorometry.Results After incubation with 10-40 μg/ml EPAfor 24-72 hours,the proliferation of human gastric cancer cells was markedly inhibited in a time-dependent manner.The treatment of 40 g/ml EPA for 72 hours increased the proportion of G0/G1 phase cells in both SGC-7901 and MGC-803 (P=0.006,P=0.009).In SGC-7901 and MGC-803 cells incubated with 40 μg/ml EPA for 24 hours,mitochondria membrane potential decreased significantly (P =0.001,P =0.047 ); cytochrome C level significantly declined in mitochondria (P=0.001,P=0.000) but increased in cytosol (P =0.001,P=0.000).In SGC-7901 cells,the apoptotic effector caspase-3 activity increased time-dependently along with incubation with 40 g/ml EPA.Conclusion EPA could inhibit the proliferation and promote the apoptosis of human gastric cancer cells through inducing cell cycle arrest and activating intrinsic death pathway mediated by mitochondria. Key words: Eicosapentaenoic acid; Stomach neoplasm; Cell cycle; Apoptosis; Mitochondria; Cytochrome C