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PPARγ Promotes Growth and Invasion of Thyroid Cancer Cells

William M Wood1, Vibha Sharma, Kevin T Bauerle

  • 1Division of Endocrinology, Metabolism and Diabetes, Department of Medicine, University of Colorado Denver, Aurora, CO 80045, USA.

PPAR Research
|December 24, 2011
PubMed

Insights

Elevated PPARγ drives aggressive thyroid cancer growth and invasiveness. Targeting PPARγ may offer a new therapeutic strategy for advanced thyroid cancer treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Undifferentiated (anaplastic) thyroid cancer (ATC) is highly aggressive with limited therapeutic options.
  • PPARγ (peroxisome proliferator-activated receptor gamma) levels are elevated in ATC cells.

Purpose of the Study:

  • To investigate the role of PPARγ in thyroid cancer progression and invasiveness.
  • To explore the therapeutic potential of targeting PPARγ in advanced thyroid cancer.

Main Methods:

  • PPARγ depletion using RNA interference in HTh74 ATC cells.
  • PPARγ overexpression in BCPAP differentiated thyroid cancer cells.
  • Assessment of cell growth, cell cycle, protein levels (pRb, cyclin A, B1), and tumor growth in vivo.
  • Evaluation of cellular invasiveness.

Main Results:

  • PPARγ depletion reduced ATC cell growth, induced cell cycle arrest, and decreased pRb and cyclin levels.
  • PPARγ depletion slowed both flank and orthotopic tumor growth.
  • PPARγ overexpression in differentiated cells increased growth and pRb/cyclin levels.
  • PPARγ depletion decreased ATC cell invasiveness, while overexpression increased invasiveness in differentiated cells.

Conclusions:

  • PPARγ plays a detrimental role in thyroid cancer, promoting growth and invasiveness.
  • Targeting PPARγ represents a potential therapeutic strategy for advanced thyroid cancer.

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