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Peroxisome proliferator‐activated receptor‐gamma ligand suppressed leptin‐mediated expression of interleukin‐8 and tumor angiogenesis in human colon cancer cells
Author(s) -
Wang FuYu,
Tang FengYao
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.931.9
Subject(s) - troglitazone , leptin , angiogenesis , cancer , colorectal cancer , cancer research , cancer cell , medicine , endocrinology , receptor , peroxisome proliferator activated receptor , umbilical vein , interleukin 8 , chemistry , cytokine , in vitro , biochemistry , obesity
Colorectal cancer is one of the leading causes of cancer death in western countries. Previous studies have demonstrated that overexpression of leptin is strongly associated with risk of human colon cancer. However, the effect of leptin on tumor angiogenesis during the development of human colon cancer has not been demonstrated well yet. The present study would investigate the role of peroxisome proliferators activated receptors (PPAR)‐gamma ligand in leptin–mediated expression of interleukin‐8 (IL‐8) and tumor angiogenesis in human colon cancer cells. Our results showed that leptin dose‐dependently (0, 0.0625, 0.25, 1 μM) induced the expression of IL‐8 in human colon cancer HT‐29 cells. Conditioned medium from leptin‐stimulated human colon cancer HT‐29 cells would also induce tubular formation in human umbilical vein endothelial cells (HUVEC). Treatment of Troglitazone (0.1 and 5μM), a specific PPAR‐ γ agonist, would suppress leptin‐mediated expression of IL‐8 in human colon cancer HT‐29 cells up to 9% and 38%, respectively. Furthermore, troglitazone–treated conditioned medium from cancer cells would suppress tubular formation in HUVEC. Take together; our results suggest that PPAR‐γ ligand could act as an important chemo‐preventive agent to suppress leptin‐mediated IL‐8 expression and tumor angiogenesis in human colon cancer. Grant Funding Source : National Science Council grant under agreement No. 97‐2320‐B‐039‐043‐MY3,