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Apoptotic effects of EGCG via AMPK/mTOR pathway and AMPK/CSK signaling on HT‐29 colon cancer cells and HepG2 hepato‐carcinoma cells
Author(s) -
Park Song Yi,
Lee YunKyoung,
Choi BuYoung,
Lee Won Sup,
Kim YoungMin,
Park Ock Jin
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.lb260
Subject(s) - ampk , pi3k/akt/mtor pathway , microbiology and biotechnology , protein kinase a , cancer research , chemistry , apoptosis , regulator , cell growth , kinase , protein kinase b , signal transduction , amp activated protein kinase , biology , biochemistry , gene
AMPK (AMP‐activated protein kinase) as an anti‐cancer target has been received attention since it functions as an upstream regulator of proliferative proteins such as tuberous sclerosis complex (TSC), mammalian target of rapamycin (mTOR), p70S6 kinase, and elongation factor‐2. Upon activation, mTOR, a cell survival molecule, exhibits uncontrolled proliferation and dysregulation of apoptosis. CSK (C‐terminal Src kinase) is an inactivator of Src and Src‐family protein kinases, proto‐oncogenes that play a role in cell survival and cell proliferation. In this study, we examined the regulation of AMPK/mTOR pathway in HT‐29 colon cancer cells and AMPK/CSK signaling in HepG2 hepato‐carcinoma cells treated with EGCG. EGCG decreased cell viability, and increased apoptotic cell death in both types of cells. The stimulation of AMPK by EGCG resulted in the down‐regulation of mTOR in HT‐29 cells and up‐regulation of CSK activities through decreasing inactive form in HepG2 cells. The application of AMPK siRNA supported the evidence that AMPK acts as an upstream signal of mTOR in cells treated with EGCG. In HepG2 cells, AMPK was found to act as a positive regulator of CSK. [This work was supported by the Korea Science and Engineering Foundation (KOSEF) grant funded by the Korea government (MEST) (NO. R01‐2008‐000‐20131‐0)]