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PPAR Research
Volume 2011, Article ID 171765, 11 pages
Research Article

PPARγ Promotes Growth and Invasion of Thyroid Cancer Cells

1Division of Endocrinology, Metabolism and Diabetes, Department of Medicine, University of Colorado Denver, Aurora, CO 80045, USA
2University of Colorado Cancer Center, University of Colorado Denver, Aurora, CO 80045, USA

Received 9 August 2011; Accepted 17 September 2011

Academic Editor: Maria Paola Cerù

Copyright © 2011 William M. Wood et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Undifferentiated (anaplastic) thyroid cancer (ATC) is one of the most aggressive human malignancies and no effective therapy is currently available. We show here that PPARγ levels are elevated in cells derived from ATC. Depletion of PPARγ in HTh74 ATC cells resulted in decreased cell growth, cell cycle arrest and a reduction in pRb and cyclin A and B1 levels. We further showed that both flank and orthotopic thyroid tumors derived from PPARγ-depleted cells grew more slowly than PPARγ-expressing cells. When PPARγ was overexpressed in more differentiated thyroid cancer BCPAP cells which lack PPARγ, there was increased growth and raised pRb and cyclin A and B1 levels. Finally, PPARγ depletion in ATC cells decreased their invasive capacity whereas overexpression in PTC cells increased invasiveness. These data suggest that PPARγ may play a detrimental role in thyroid cancer and that targeting it therapeutically may lead to improved treatment of advanced thyroid cancer.