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Glucocorticoids induce CCN5/WISP-2 expression and attenuate invasion in oestrogen receptor-negative human breast

Nathalie Ferrand1, Emilien Stragier, Gérard Redeuilh

  • 1Cancer Biology and Therapeutics, Centre de Recherche Saint-Antoine, Paris, France.

The Biochemical Journal
|July 7, 2012
PubMed

Insights

Glucocorticoids induce CCN5 expression in aggressive ER-negative breast cancer cells, promoting a less invasive epithelial phenotype. This suggests a new therapeutic strategy for high-risk breast cancer patients.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Endocrinology

Background:

  • CCN5 (WISP-2) is an oestrogen-regulated CCN family member that represses epithelial-mesenchymal transition (EMT) genes, maintaining differentiation in ER-positive breast cancer.
  • CCN5 is typically absent in aggressive ER-negative breast cancer cells.

Purpose of the Study:

  • To investigate the effect of glucocorticoids on CCN5 expression and phenotype in ER-negative breast cancer cells.
  • To explore the potential of glucocorticoid-induced CCN5 as a therapeutic strategy for aggressive breast cancer.

Main Methods:

  • Treatment of MDA-MB-231 (ER-negative) and ER-positive breast cancer cells with glucocorticoids.
  • Analysis of CCN5 gene promoter activity and glucocorticoid receptor interaction.
  • Assessment of cellular morphology, invasiveness, and expression of EMT markers (vimentin, cadherin 11, ZEB1).
  • Evaluation of oestrogen receptor (ER) expression in response to glucocorticoids.

Main Results:

  • Glucocorticoid exposure induced CCN5 expression in ER-negative MDA-MB-231 cells via glucocorticoid-response element interaction.
  • Glucocorticoid treatment reduced invasiveness and mesenchymal marker expression in MDA-MB-231 cells, alongside morphological changes.
  • In ER-positive cells, glucocorticoids down-regulated ER expression, inhibiting oestrogen signalling, without increasing CCN5.
  • Glucocorticoid treatment of ER-negative cells led to increased CCN5 and a more differentiated, less invasive epithelial phenotype.

Conclusions:

  • Glucocorticoid treatment can induce CCN5 expression in ER-negative breast cancer, shifting cells towards a less aggressive epithelial phenotype.
  • This mechanism offers a potential novel therapeutic approach for high-risk breast cancer patients.
  • CCN5 induction by glucocorticoids represents a promising strategy to counteract EMT and reduce invasiveness in aggressive breast cancers.

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