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Prolonged sulforaphane treatment activates extracellular‐regulated kinase 1/2 signaling in nontumorigenic colon cells but not colon cancer cells
Author(s) -
Zeng Huawei,
Trujillo Olivia,
Moyer Mary P.,
Botnen James H.
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.928.4
Subject(s) - sulforaphane , apoptosis , cancer research , kinase , cell growth , colorectal cancer , chemistry , mapk/erk pathway , cell cycle , cell , microbiology and biotechnology , cancer , biology , medicine , biochemistry
Sulforaphane (SFN) is a naturally occurring member of the isothiocyanate family of chemopreventive agents and the induction of cell cycle arrest and apoptosis is a key mechanism by which SFN exerts its colon cancer prevention. However, little is known about the differential effects of SFN on colon cancer and normal cells. In this study, we demonstrated that prolonged SFN (5, 10 or 15 _mol/L) exposure (72 h) inhibited cell proliferation up to 95% in colon cancer cells (HCT116) and 52% in normal colon mucosa‐derived (NCM460) cells, respectively. Our data also showed that prolonged SFN exposure led to the significant induction of apoptosis and G 2 /M cell cycle arrest in HCT116, but to a much lesser extent in NCM460 cells. Furthermore, the examination of mitogen‐activated protein kinase (MAPK) signaling status revealed that prolonged SFN treatment strongly up‐regulated the extracellular‐regulated kinase ½ (ERK1/2) in NCM460 but not HCT116 cells. Taken together, the activation of ERK1/2 in NCM460 but not HCT116 cells may play a critical role in SFN's stronger potential of inhibiting colon cancer cell proliferation when compared with normal colon cells. Supported by USDA/ARS