Open AccessPPARγ
Author(s) -
William M. Wood,
Vibha Sharma,
Kevin T. Bauerle,
Laura A. Pike,
Qiong Zhou,
Deborah Fretwell,
Rebecca E. Schweppe,
Bryan R. Haugen
Publication year - 2011
Publication title -
ppar research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 49
eISSN - 1687-4765
pISSN - 1687-4757
DOI - 10.1155/2011/171765
Subject(s) - cancer research , cell growth , thyroid cancer , thyroid , peroxisome proliferator activated receptor , anaplastic thyroid cancer , medicine , algorithm , endocrinology , receptor , chemistry , mathematics , biochemistry
Undifferentiated (anaplastic) thyroid cancer (ATC) is one of the most aggressive human malignancies and no effective therapy is currently available. We show here that PPAR γ levels are elevated in cells derived from ATC. Depletion of PPAR γ 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 PPAR γ -depleted cells grew more slowly than PPAR γ -expressing cells. When PPAR γ was overexpressed in more differentiated thyroid cancer BCPAP cells which lack PPAR γ , there was increased growth and raised pRb and cyclin A and B1 levels. Finally, PPAR γ depletion in ATC cells decreased their invasive capacity whereas overexpression in PTC cells increased invasiveness. These data suggest that PPAR γ may play a detrimental role in thyroid cancer and that targeting it therapeutically may lead to improved treatment of advanced thyroid cancer.
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