Epigallocatechin-3-gallate inhibits growth and induces apoptosis in esophageal cancer cells through the demethylation and reactivation of the p16 gene.

The present study aimed to investigate the effect of treatment with epigallocatechin-3-gallate (EGCG) on the human esophageal cancer cell line ECa109 and elucidate the associated underlying mechanisms. ECa109 cells were cultured and treated with increasing concentrations of EGCG for various durations. Cell viability was evaluated using the MTT assay and apoptosis was detected using flow cytometry. The methylation status of the cyclin-dependent kinase inhibitor 2A (p16) gene was analyzed using the methylation-specific polymerase chain reaction (PCR). p16 mRNA and protein expression was measured using reverse transcription-quantitative PCR and western blot analysis, respectively. The results of the present study demonstrated that, following treatment with EGCG, ECa109 cell viability was significantly decreased, while the rate of apoptosis was significantly increased (P<0.01), in a dose- and time-dependent manner. Following treatment of ECa109 cells with EGCG, p16 gene demethylation, and its mRNA and protein expression, were significantly increased compared with the untreated cells (P<0.01). EGCG may induce ECa109 cell apoptosis and inhibit cell growth through p16 gene demethylation, which restores its expression.