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Orphan receptors COUP-TF and DAX-1 as targets in disordered CYP17 expression in adrenocortical tumors

H Shibata1, Y Ikeda, K Morohashi

  • 1Health Center and Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan. hiro-405@cb3.so-net.ne.jp

Endocrine Research
|February 24, 2001
PubMed

Insights

The study found that the expression of orphan receptors COUP-TF and DAX-1 is inversely related to CYP17 gene expression in adrenocortical tumors. This suggests their role in excessive hormone production in these tumors.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Oncology

Background:

  • CYP17 gene transcription is regulated by SF-1, COUP-TF, and DAX-1 orphan receptors.
  • SF-1 activates transcription, while COUP-TF and DAX-1 inhibit it.
  • The role of these receptors in adrenocortical tumors is not fully understood.

Purpose of the Study:

  • To investigate the expression levels of SF-1, COUP-TF, and DAX-1 in adrenocortical tumors.
  • To correlate the expression of these orphan receptors with CYP17 expression.
  • To determine the pathophysiologic role of these receptors in excessive hormone production in adrenocortical tumors.

Main Methods:

  • Analysis of orphan receptor and CYP17 gene expression in cortisol-producing and deoxycorticosterone-producing adenomas.
  • Comparison of expression levels between tumor types and with normal adrenal tissue (implied).

Main Results:

  • CYP17 was highly expressed in cortisol-producing adenomas, with low COUP-TF and DAX-1.
  • CYP17 was lowly expressed in deoxycorticosterone-producing adenomas, with high DAX-1 and decreased SF-1.
  • Reciprocal expression patterns observed between CYP17 and transcriptional repressors COUP-TF and DAX-1.

Conclusions:

  • The findings suggest a pathophysiologic role for COUP-TF and DAX-1 in adrenocortical tumors.
  • Reciprocal expression of CYP17 and these repressors indicates their involvement in excessive hormone production.
  • Further research into these molecular mechanisms could lead to novel therapeutic strategies.

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