RORα suppresses breast tumor invasion by inducing SEMA3F expression

Gaofeng Xiong1, Chi Wang, B Mark Evers

  • 1Markey Cancer Center, and the Department of Molecular and Biomedical Pharmacology, Surgery, and Molecular and Cellular Biochemistry, University of Kentucky, Lexington, Kentucky 40536, USA.

Cancer Research
|February 22, 2012
PubMed

Insights

Retinoid orphan nuclear receptor alpha (RORα) acts as a tumor suppressor by regulating semaphorin 3F (SEMA3F), inhibiting breast cancer invasion and improving prognosis. Restoring RORα expression reduces tumor growth and enhances SEMA3F levels.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Breast cancer invasion requires inactivating tumor suppressors and microenvironmental factors.
  • Identifying these factors is crucial for understanding breast cancer and developing therapies.

Purpose of the Study:

  • To identify novel tumor suppressors and microenvironmental factors involved in breast cancer invasion.
  • To investigate the role of retinoid orphan nuclear receptor alpha (RORα) and semaphorin 3F (SEMA3F) in breast cancer progression.

Main Methods:

  • Analysis of gene expression profiles in 3D culture models of human mammary epithelial cells.
  • Chromatin immunoprecipitation and luciferase reporter assays to determine RORα's regulatory role.
  • In vivo studies using nude mice to assess tumor growth inhibition.

Main Results:

  • RORα was identified as a regulator of SEMA3F, a suppressive microenvironmental factor.
  • RORα and SEMA3F expression were downregulated in human breast cancer tissues and correlated with poor prognosis.
  • Restoring RORα expression in cancer cells inhibited tumor growth, enhanced SEMA3F, and promoted non-invasive structures.
  • RORα directly regulates SEMA3F transcription, and SEMA3F is essential for RORα's tumor-suppressive effects.

Conclusions:

  • RORα functions as a tumor suppressor by inducing a suppressive microenvironment via SEMA3F.
  • RORα-SEMA3F signaling represents a potential therapeutic target for inhibiting breast cancer invasion.