Open AccessPeroxisome Proliferator‐activated Receptor γ Induces Growth Arrest and Differentiation Markers of Human Colon Cancer Cells
Author(s) -
Kitamura Shinji,
Miyazaki Yoshiji,
Shinomura Yasuhisa,
Kondo Shinya,
Kanayama Shuji,
Matsuzawa Yuji
Publication year - 1999
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.1999.tb00668.x
Subject(s) - troglitazone , peroxisome proliferator activated receptor , biology , cellular differentiation , adipocyte , receptor , cell growth , endocrinology , microbiology and biotechnology , medicine , cancer research , adipose tissue , biochemistry , gene
Peroxisome proliferator‐activated receptor γ (PPARγ), one of the nuclear receptors expressed in adipose tissue, plays an important role in adipocyte differentiation. In this study, we investigated the expression of PPARγ and its role in cellular growth and differentiation in six colon cancer cell lines: HT‐29, CaCo‐2, SW‐480, DLD‐1, LoVo, and T‐84. All six expressed PPARγ mRNA and protein, shown respectively on northern and western blot analyses. Luciferase assay in HT‐29 cells, which strongly express PPARγ showed that troglitazone, a selective ligand for PPAR?, transacti‐vated the transcription of a peroxisome proliferator response element (PPRE)‐driven promoter. Furthermore, troglitazone caused a marked decrease in [ 3 H] thymidine incorporation and G1 cell‐cycle arrest determined by flow cytometry. Finally, troglitazone induced expression of mRNAs for villin and intestinal alkaline phosphatase, markers for enterocyte differentiation. In conclusion, human colon cancer cells express PPARγ, the ligands of which inhibit cell growth and induce differentiation markers.