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Chrysophanic acid blocks proliferation of colon cancer cells by inhibiting EGFR/mTOR pathway
Author(s) -
Lee Myung Sun,
Cha Eun Young,
Sul Ji Young,
Song In Sang,
Kim Ji Yeon
Publication year - 2011
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.3323
Subject(s) - pi3k/akt/mtor pathway , ribosomal protein s6 , protein kinase b , cancer research , cell growth , epidermal growth factor receptor , signal transduction , rptor , kinase , ribosomal s6 kinase , chemistry , phosphorylation , epidermal growth factor , microbiology and biotechnology , biology , p70 s6 kinase 1 , biochemistry , receptor
Inactivation of epidermal growth factor receptor (EGFR) is a prime method used in colon cancer therapy. Here it is shown that chrysophanic acid, a natural anthraquinone, has anticancer activity in EGFR‐overexpressing SNU‐C5 human colon cancer cells. Chrysophanic acid preferentially blocked proliferation in SNU‐C5 cells but not in other cell lines (HT7, HT29, KM12C, SW480, HCT116 and SNU‐C4) with low levels of EGFR expression. Chrysophanic acid treatment in SNU‐C5 cells inhibited EGF‐induced phosphorylation of EGFR and suppressed activation of downstream signaling molecules, such as AKT, extracellular signal‐regulated kinase (ERK) and the mammalian target of rapamycin (mTOR)/ribosomal protein S6 kinase (p70S6K). Chrysophanic acid (80 and 120 µ m ) significantly blocked cell proliferation when combined with the mTOR inhibitor, rapamycin. These findings offer the first evidence of anticancer activity for chrysophanic acid via EGFR/mTOR mediated signaling transduction pathway. Copyright © 2010 John Wiley & Sons, Ltd.