The Effect of Different Treatments of (–)-Epigallocatechin-3-Gallate on Colorectal Carcinoma Cell Lines. (3rd October 2018)

• Record Type: Journal Article
• Authors: Ding, Yang-Ping; Gao, Zi-Li; Chen, Bing-Can; Rakariyatham, Kanyasiri; Suo, Hua-Yi; Tong, Hua-Rong; Xiao, Hang
• Is Part Of: Nutrition and cancer. Volume 70:Number 7(2018)
• Page Start: 1126
• Page End: 1136
• Publication Date: 2018-10-03
• Subjects: Cancer -- Periodicals; Nutrition -- Periodicals; Cancer; Nutrition; Periodicals; 616.9940654
• DOI: 10.1080/01635581.2018.1497671
• Languages: English
• ISSNs: 0163-5581

Abstract

Abstract: Backgroud: (-)-Epigallocatechin-3-gallate (EGCG), the major component of green tea, is well documented to induce apoptosis and cell cycle arrest in cancer by targeting multiple signal transduction pathways. However, EGCG is extremely unstable in general culture conditions and rapidly degraded. So, to what extent EGCG or which degradation products of EGCG play a role in anti-tumor is still unknown. In this study, we evaluated the effect of different treatments of EGCG on HCT116 cells. Design: MTT assay was applied to evaluated the inhibitory effect of different treatments of EGCG on HCT116 cells. Cell cycle and apoptosis were performed by flow cytometry. Finally, western blot analysis was used to elucidate the molecular mechanism associated with cell cycle arrest and apoptosis. Results: Compared with control, both EGCG and O-EGCG (i.e., EGCG being pre-incubated at 37°C for 3 h) significantly inhibited HCT116 cells growth. Surprisingly, we found that the inhibitory effect of O-EGCG was stronger than that of EGCG. The IC50 values of EGCG and O-EGCG were 8.75 and 5.40 μM, respectively. Cell cycle analysis showed that 20 μM of EGCG simultaneously caused cell cycle arrest at G1 and G2 phase in HCT116 cells, differing from O-EGCG which exclusively caused cell cycle arrest at G2. This result suggested that parent EGCG at the early treatment might cause cell cycle arrest at G1. As time went on, EGCG disappeared and degraded products of EGCG were formed which might cause cell cycle arrest at G2. Further studies revealed that EGCG induced cell cycle arrest at G1 by downregulation of cyclin E and cyclin D1 and upregulation of p21. On the other hand, O-EGCG induced HCT116 cells apoptosis mainly by increasing the expression of p53 and cleaved caspase-3, which might be the underlying reason why O-EGCG had stronger inhibitory effect on HCT116 cells line than EGCG. Conclusions: The pretreatment of EGCG may be an effective way to enhance its antitumor effect.