15-hydroxy-eicosatetraenoic acid arrests growth of colorectal cancer cells via a peroxisome proliferator-activated receptor gamma-dependent pathway
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AbstractPeroxisome proliferator-activated receptor gamma (PPARgamma) inhibits cell growth via promoting apoptosis. Human colorectal cancer tissues had abundant PPARgamma but the incidence of apoptosis was very low, suggesting a defect in the PPARgamma pathway. Here, we found that 15-hydroxy-eicosatetraenoic acid (15S-HETE), an endogenous ligand for PPARgamma, was significantly decreased in the serum of patients with colorectal cancer. Treatment of colon cancer cells with 15S-HETE inhibited cell proliferation and induced apoptosis, which was preceded by an increase in TGF-beta-inducible early gene (TIEG) and a decrease in Bcl-2. The action of 15S-HETE could be blocked when PPARgamma was suppressed. Overexpression of Bcl-2 prevented the apoptosis. The levels of TIEG and 15-lipoxygenase (15-LOX), the enzyme responsible for 15S-HETE production, was decreased in colorectal cancer. Therefore, colorectal cancer is associated with decreased 15S-HETE. Treatment of colon cancer cells with 15S-HETE inhibits cell proliferation and induces apoptosis in a PPARgamma-dependent pathway involving augmentation of TIEG and reduction of Bcl-2 expression. (C) 2003 Wiley-Liss, Inc.
All Author(s) ListChen GG, Xu H, Lee JFY, Subramaniam M, Leung KL, Wang SH, Chan UPF, Spelsberg TC
Volume Number107
Issue Number5
Pages837 - 843
LanguagesEnglish-United Kingdom
Keywords15-lipokygenase; colorectal carcinoma; peroxisome proliferator-activated receptor gamma 15-hydroxy-eicosatetraenoic acid; TGF-beta-inducible early gene and Bcl-2
Web of Science Subject CategoriesOncology; ONCOLOGY

Last updated on 2020-19-01 at 02:45