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[Cancer Research 64, 5994-6001, September 1, 2004]
© 2004 American Association for Cancer Research

Regular Articles

1,1-Bis(3'-indolyl)-1-(p-substitutedphenyl)methanes Induce Peroxisome Proliferator-Activated Receptor {gamma}-Mediated Growth Inhibition, Transactivation, and Differentiation Markers in Colon Cancer Cells

Sudhakar Chintharlapalli1, Roger Smith, III2, Ismael Samudio3,4, Wei Zhang5 and Stephen Safe3,4

1 Departments of Biochemistry and Biophysics, 2 Veterinary Pathobiology, and 3 Veterinary Physiology and Pharmacology, Texas A&M University, College Station, Texas; 4 Institute of Biosciences and Technology, Texas A&M University System Health Science Center, Houston, Texas; and 5 Division of Pathology and Laboratory Medicine, M. D. Anderson Cancer Center, Houston, Texas

1,1-Bis(3'indolyl)-1–(p-substitutedphenyl)methanes containing p-trifluoromethyl (DIM-C-pPhCF3), p-t-butyl (DIM-C-pPhtBu), and p-phenyl (DIM-C-pPhC6H5) groups induce peroxisome proliferator-activated receptor {gamma} (PPAR{gamma})-mediated transactivation in HT-29, HCT-15, RKO, and SW480 colon cancer cell lines. Rosiglitazone also induces transactivation in these cell lines and inhibited growth of HT-29 cells, which express wild-type PPAR{gamma} but not HCT-15 cells, which express mutant (K422Q) PPAR{gamma}. In contrast, DIM-C-pPhCF3, DIM-C-pPhtBu, and DIM-C-pPhC6H5 inhibited growth of both HT-29 and HCT-15 cells with IC50 values ranging from 1 to 10 µmol/L. Rosiglitazone and diindolylmethane (DIM) analogues did not affect expression of cyclin D1, p21, or p27 protein levels or apoptosis in HCT-15 or HT-29 cells but induced keratin 18 in both cell lines. However, rosiglitazone induced caveolins 1 and 2 in HT-29 but not HCT-15 cells, whereas these differentiation markers were induced by DIM-C-pPhCF3 and DIM-C-pPhC6H5 in both cell lines. Because overexpression of caveolin 1 is known to suppress colon cancer cell and tumor growth, the growth inhibitory effects of rosiglitazone and the DIM compounds are associated with PPAR{gamma}-dependent induction of caveolins.




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