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[Cancer Research 63, 5274-5280, September 1, 2003]
© 2003 American Association for Cancer Research

Regular Articles

Mutant Thyroid Hormone Receptor ß Represses the Expression and Transcriptional Activity of Peroxisome Proliferator-activated Receptor {gamma} during Thyroid Carcinogenesis

Hao Ying, Hideyo Suzuki, Li Zhao, Mark C. Willingham, Paul Meltzer and Sheue-Yann Cheng1

Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland 20892-4264 [H. Y., H. S., L. Z., S-Y. C.]; National Human Genome Research Institute, NIH, Bethesda, Maryland 20892-4264 [P. M.]; and Department of Pathology, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157-1072 [M. C. W.]

The molecular genetics underlying thyroid carcinogenesis is not clear. Recent identification of a PAX8-peroxisome proliferator-activated receptor {gamma} (PPAR{gamma}) fusion gene in human thyroid follicular carcinoma suggests a tumor suppressor role of PPAR{gamma} in thyroid carcinogenesis. Mice harboring a knockin mutant thyroid hormone ß receptor (TRßPV) spontaneously develop thyroid follicular carcinoma through pathological progression of hyperplasia, capsular invasion, vascular invasion, anaplasia, and eventually, distant organ metastasis. This mutant mouse (TRßPV/PV mouse) provides an unusual opportunity to ascertain the role of PPAR{gamma} in thyroid carcinogenesis. Here, we show that the expression of PPAR{gamma} mRNA was repressed in the thyroid gland of mutant mice during carcinogenesis. In addition, TRßPV acted to abolish the ligand (troglitazone)-mediated transcriptional activity of PPAR{gamma}. These results indicate that repression of PPAR{gamma} expression and its transcriptional activity are associated with thyroid carcinogenesis and raise the possibility that PPAR{gamma} could be tested as a therapeutic target in thyroid follicular carcinoma.




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