The effect of eicosapentaenoic acid on the proliferation and apoptosis of gastric cancer cells
10.3760/cma.j.issn.1674-635X.2012.02.006
- VernacularTitle:二十碳五烯酸(EPA)对胃癌细胞增殖与凋亡的影响
- Author:
Yong YIN
;
Yulong HE
;
Shirong CAI
;
Wenhua ZHAN
- Publication Type:Journal Article
- Keywords:
Eicosapentaenoic acid;
Stomach neoplasm;
Cell cycle;
Apoptosis;
Mitochondria;
Cytochrome C
- From:
Chinese Journal of Clinical Nutrition
2012;20(2):88-92
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo observe the effect of eicosapentaenoic acid (EPA) on the proliferation and apoptosis of human gastric cancer cells and to explore the potential mechanism involved.MethodsHuman 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.ResultsAfter 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.ConclusionEPA 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.
