Effects of EGCG on proliferation and apoptosis of gastric cancer SGC7901 cells via down-regulation of HIF-1α and VEGF under a hypoxic state.

Abstract

To investigate the effects of epigallocatechin-3-gallate (EGCG) on proliferation and apoptosis of human gastric cancer SGC7901 cells under a hypoxic state. Human gastric cancer SGC7901 cells were sub-cultured, and the cobalt chloride (CoCl2) hypoxia model was established. The blank control group (normoxia group), hypoxia control group (hypoxia group) and hypoxia + different concentrations of EGCG subgroups (20, 40, 60, 80, 100 μg/mL EGCG) were set up. Cell viability was detected via methyl thiazolyl tetrazolium (MTT) assay, apoptosis was detected via flow cytometry, and expressions of hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) were detected via reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting. Relatively low concentrations of EGCG (20-80 μg/mL) presented no significant inhibiting effect on SGC7901 cell growth within a short time (24 h) (p>0.05). The increasing concentration of EGCG inhibited cell proliferation under a hypoxia state (p<0.05). EGCG induced apoptosis in a dose-dependent manner under hypoxia (p<0.05). EGCG could significantly impede expressions of HIF-1α and VEGF proteins (p<0.05), and down-regulate the level of VEGF mRNA (p<0.05), but it showed no significant effect on the HIF-1α mRNA expression (p>0.05). EGCG inhibited cell proliferation under hypoxia via the downregulation of HIF-1α and its downstream target gene VEGF levels, providing a theoretical basis for the early diagnosis and treatment of gastric cancer in clinic.