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Orphan receptor small heterodimer partner suppresses tumorigenesis by modulating cyclin D1 expression and cellular

Yuxia Zhang1, Ping Xu, Kyungtae Park

  • 1Department of Medicine and Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, UT 84132, USA.

Hepatology (Baltimore, Md.)
|June 10, 2008
PubMed
Abstract

Insights

Small heterodimer partner (SHP) acts as a tumor suppressor by inhibiting cell growth. SHP deficiency in mice and cells promotes liver cancer and uncontrolled proliferation via cyclin D1 regulation.

Area of Science:

  • Hepatology
  • Molecular Biology
  • Oncology

Background:

  • The small heterodimer partner (SHP; NROB2) is a nuclear receptor involved in liver function.
  • The role of SHP in cellular proliferation and tumorigenesis remains unexplored.

Purpose of the Study:

  • To investigate the function of SHP in cellular proliferation and tumorigenesis.
  • To determine if SHP acts as a tumor suppressor.

Main Methods:

  • Studied SHP knockout (SHP-/-) and SHP-transgenic mice.
  • Analyzed SHP-/- embryonic fibroblasts in vitro.
  • Assessed cyclin D1 expression and gene transcription.
  • Evaluated tumor formation in nude mice.

Main Results:

  • SHP-/- mice developed spontaneous hepatocellular carcinoma with increased hepatocyte proliferation and cyclin D1.
  • SHP overexpression reversed these effects.
  • SHP-/- fibroblasts exhibited enhanced proliferation, increased cyclin D1 mRNA and protein, and formed tumors in vivo.
  • SHP directly represses cyclin D1 gene transcription.

Conclusions:

  • SHP exhibits tumor suppressor functions.
  • SHP negatively regulates cellular growth, thereby inhibiting tumorigenesis.

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