Inhibitory effect and mechanism of(－)-epigallocatechin-3-gallate on HT29 and HCT-8 colorectal cancer cell lines and expression of HES1 and JAG1

/Zhang Chunxia

(張春霞，National Cent Surg Colorectal，3rd Affil Hosp Nanjing Univ Tradit Chin Med，Jiangsu Integ Colorectal Oncol Center，Nanjing 210001)…∥Chin J Gastrointest Surg.-2011，14(8).-636 ～639

ObjectiveTo study the inhibitory effect of(-)-epigallocatechin-3-gallate(EGCG)on cancer cells line HCT-8 and HT29 and its influence on the expression of HES1 and JAG1.MethodsColorectal cancer cells line HCT-8 and HT29 were cultured in vitro and treated with different concentrations of EGCG(10 mg/L，20 mg/L，35 mg/L).The inhibition of proliferation was tested by MTT analysis.Influence of EGCG on the cell apoptosis and cell cycle of HCT-8 and HT29 were detected with flow cytometry，and gene expression of HCT-8 and HT29 after EGCG treatment with real-time polymerase chain reaction.ResultsEGCG affected the proliferation and apoptosis of HCT-8 and HT29.The inhibition rates of the three different concentrations of EGCG were(28.894 ±5.076)%，(34.903 ± 1.794)%，and(39.028 ±0.105)%on HCT-8，and(14.682 ± 4.244)%，(22.429 ±3.847)%，and(29.840 ± 5.076)%on HT29.EGCG caused G2/M phase arrest and M phase transition in HCT-8 cell line，and S phase arrest and G2 phase transition in HT29 cell line.EGCG down-regulated HES1 gene expression in both cell fines，however，the differences were not statistically significant(both P ＞0.05).EGCG upregulated JAG1 gene expression in both cell lines，however only the difference in HCT-8 was statistically significant(0.201 ±0.018 vs.0.440 ±0.077，P=0.029).ConclusionEGCG can significantly inhibit the proliferation of HT29 cells and HCT-8 cells by changing cell cycle and inducing cell apoptosis.The mechanism may be related to the upregulation of JAG1 gene expression.11 refs，2 figs，2 tabs.