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CCN6 (WISP3) as a new regulator of the epithelial phenotype in breast cancer

Celina G Kleer1, Yanhong Zhang, Sofia D Merajver

  • 1Department of Pathology, Division of Hematology/Oncology, University of Michigan Medical School, Ann Arbor, Mich. 48109, USA. kleer@umich.edu

Cells, Tissues, Organs
|June 26, 2007
PubMed

Insights

CCN6 (WISP3) protein levels are reduced in inflammatory breast cancer, a lethal cancer type. Loss of CCN6 promotes epithelial-mesenchymal transition (EMT), crucial for cancer progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • CCN6 (WISP3) is a secreted protein in the CCN gene family.
  • It exhibits tumor growth, proliferation, and invasion inhibitory functions in breast cancer.
  • CCN6 mRNA is reduced in 80% of locally advanced inflammatory breast cancer cases.

Purpose of the Study:

  • To review the function of CCN6 in breast cancer.
  • To emphasize CCN6's role in regulating epithelial phenotype and E-cadherin expression.

Main Methods:

  • Review of existing literature on CCN6 function in breast cancer.
  • Analysis of CCN6's role in epithelial-mesenchymal transition (EMT) induction.
  • Investigation of CCN6's impact on E-cadherin gene expression.

Main Results:

  • CCN6 deficiency is linked to reduced E-cadherin expression.
  • Downregulation of CCN6 in mammary epithelial cells induces EMT.
  • CCN6 acts as a regulator of the epithelial phenotype in breast cancer.

Conclusions:

  • CCN6 plays a critical role in maintaining the epithelial phenotype in breast cancer.
  • CCN6's function as a tumor suppressor is linked to its regulation of EMT and E-cadherin.
  • Further research into CCN6 could offer new therapeutic strategies for inflammatory breast cancer.

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