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Regulation of differential COUP-TF-coregulator interactions in adrenal cortical steroidogenesis

Hirotaka Shibata1, Isao Kurihara, Sakiko Kobayashi

  • 1Health Center, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. hiro405@cb3.so-net.ne.jp

Insights

Decreased expression of Chicken ovalbumin upstream promoter-transcription factors (COUP-TFs) is linked to CYP17 overexpression in cortisol-producing adenomas. A novel coregulator suggests COUP-TFs have bifunctional roles in gene regulation.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Hyperfunctioning adrenocortical adenomas involve excessive corticosteroid production due to dysregulated steroidogenic enzyme expression.
  • Transcriptional dysregulation, rather than genetic mutations, is suspected as the cause of altered enzyme activity.

Purpose of the Study:

  • To investigate the role of Chicken ovalbumin upstream promoter-transcription factors (COUP-TFs) and steroidogenic factor-1 (SF-1) in the transcriptional regulation of steroidogenic genes in adrenocortical adenomas.
  • To identify potential coregulators of COUP-TFs involved in tumor development.

Main Methods:

  • Transfection studies using Y-1 cells to analyze the interaction between SF-1 and COUP-TFs on the CYP17 gene promoter.
  • Quantitative analysis of COUP-TFI and COUP-TFII expression in cortisol-producing adenomas.
  • Yeast two-hybrid screening to identify proteins interacting with COUP-TFI.

Main Results:

  • COUP-TFs repress SF-1 transcriptional activity on the CYP17 promoter, indicating a negative regulatory role.
  • Expression of COUP-TFI and COUP-TFII is significantly decreased in cortisol-producing adenomas with high CYP17 expression.
  • A novel RING finger-containing protein interacting with COUP-TFI was identified, which can act as a coregulator.

Conclusions:

  • Reduced expression of COUP-TFs contributes to CYP17 overexpression in cortisol-producing adenomas.
  • COUP-TFI exhibits bifunctional transcriptional activity (activation and repression) depending on promoter context and coregulators, as exemplified by its opposing effects on CYP17 and CYP11B2 promoters.

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