Expression of TRPC6 channels in human epithelial breast cancer cells

Arnaud Guilbert, Isabelle Dhennin-Duthille, Yassine E.L. Hiani, Nathalie Haren, Hafida Khorsi, Henri Sevestre, Ahmed Ahidouch, Halima Ouadid-Ahidouch

Résultat de recherche: Articleexamen par les pairs

84 Citations (Scopus)

Résumé

Background: TRP channels have been shown to be involved in tumour generation and malignant growth. However, the expression of these channels in breast cancer remains unclear. Here we studied the expression and function of endogenous TRPC6 channels in a breast cancer cell line (MCF-7), a human breast cancer epithelial primary culture (hBCE) and in normal and tumour breast tissues. Methods: Molecular (Western blot and RT-PCR), and immunohistochemical techniques were used to investigate TRPC6 expression. To investigate the channel activity in both MCF-7 cells and hBCE we used electrophysiological technique (whole cell patch clamp configuration). Results: A non selective cationic current was activated by the oleoyl-2-acetyl-sn-glycerol (OAG) in both hBCE and MCF-7 cells. OAG-inward current was inhibited by 2-APB, SK&F 96365 and La3+. TRPC6, but not TRPM7, was expressed both in hBCE and in MCF-7 cells. TRPC3 was only expressed in hBCE. Clinically, TRPC6 mRNA and protein were elevated in breast carcinoma specimens in comparison to normal breast tissue. Furthermore, we found that the overexpression of TRPC6 protein levels were not correlated with tumour grades, estrogen receptor expression or lymph node positive tumours. Conclusion: Our results indicate that TRPC6 channels are strongly expressed and functional in breast cancer epithelial cells. Moreover, the overexpression of these channels appears without any correlation with tumour grade, ER expression and lymph node metastasis. Our findings support the idea that TRPC6 may have a role in breast carcinogenesis.

Langue d'origineEnglish
Numéro d'article125
JournalBMC Cancer
Volume8
DOI
Statut de publicationPublished - mai 2 2008
Publié à l'externeOui

Note bibliographique

Funding Information:
Financial support for the research described in this article was provided by the Région Picardie, Cancéropôle Nord-Ouest (INCa), Ligue contre le Cancer, the Ministère de l Education Nationale and ARC (Association pour la Recherche sur le Cancer). We thank Jean François Lefebvre for his excellent technical assistance as well as staff at the Amiens hospital.

ASJC Scopus Subject Areas

  • Oncology
  • Genetics
  • Cancer Research

PubMed: MeSH publication types

  • Journal Article
  • Research Support, Non-U.S. Gov't

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