Control of AMP-activated protein kinase, Akt, and mTOR in EGCG-treated HT-29 colon cancer cells

Suppressing the mammalian target of rapamycin (mTOR) pathway has emerged as an attractive method for controlling cancer growth and preventing cancers. Epigallocatechin-3-gallate (EGCG) is a well-known chemopreventive polyphenol, and its effects on AMP-activated protein kinase (AMPK) activation were previously reported. In this study the regulatory mechanisms of EGCG on mTOR and Akt, 2 cancer survival signals, and the interrelationships among mTORC1, Akt, and AMPK were examined. It was found that the suppression of mTORC1 by EGCG requires signals from AMPK, however, the inhibition of Akt with EGCG seems to be AMPK independent. Further, there was no clear indication of Akt as an upstream regulator of mTOR in EGCG treated HT-29 colon cancer cells.