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PGC-1-related coactivator and targets are upregulated in thyroid oncocytoma

Frédérique Savagner1, Delphine Mirebeau, Caroline Jacques

  • 1INSERM EMI-U 00-18, Laboratoire de Biochimie et Biologie Moléculaire, CHU, Angers, France. frsavagner@chu-angers.fr

Biochemical and Biophysical Research Communications
|October 11, 2003
PubMed

Insights

Thyroid oncocytomas show increased mitochondria due to overexpression of the PGC-1 related coactivator (PRC) pathway. This pathway drives mitochondrial proliferation in these thyroid tumors.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Oncology

Background:

  • Thyroid oncocytomas are characterized by excessive mitochondrial accumulation.
  • The precise cause of this mitochondrial hyperplasia remains unclear.
  • The PGC-1 coactivator family regulates mitochondrial biogenesis by activating nuclear genes for mitochondrial proteins.

Purpose of the Study:

  • To investigate the role of the PGC-1 related coactivator (PRC) in the mitochondrial proliferation observed in thyroid oncocytomas.
  • To quantify the expression of PRC, NRF-1, and TFAM in oncocytic tumors and normal thyroid tissue.

Main Methods:

  • Gene expression analysis of PRC, NRF-1, and TFAM transcripts.
  • Measurement of cytochrome oxidase activity.
  • Quantification of mitochondrial DNA (mtDNA) content.
  • Analysis of 30 oncocytic tumors and matched normal thyroid tissues.

Main Results:

  • Significant overexpression of PRC, NRF-1, and TFAM transcripts was observed in thyroid oncocytomas compared to normal tissues.
  • Increased cytochrome oxidase activity and mtDNA content were found in the tumors.
  • No specific mtDNA variants in the D-loop region were implicated in oncocytoma development.

Conclusions:

  • Overexpression of the PRC pathway is identified as the driving factor for mitochondrial proliferation in thyroid oncocytomas.
  • The PRC pathway plays a crucial role in the pathogenesis of these tumors.

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