Research article

Expression of TRPC6 channels in human epithelial breast cancer cells

Arnaud Guilbert^1†, Isabelle Dhennin-Duthille^1†, Yassine EL Hiani¹, Nathalie Haren¹, Hafida Khorsi², Henri Sevestre^3,1, Ahmed Ahidouch^4,1 and Halima Ouadid-Ahidouch^1*

• * Corresponding author: Halima Ouadid-Ahidouch ha-sciences@u-picardie.fr

• † Equal contributors

Author Affiliations

¹ Laboratoire de Physiologie Cellulaire et Moléculaire, JE « Canaux ioniques dans le cancer du sein », Faculté des Sciences, Université de Picardie Jules Verne, 33 Rue St Leu 80039, Amiens, France

² Dysrégulations Métaboliques Acquises et Génétiques, Faculté de Médecine, Université de Picardie Jules Verne, 3 rue des Louvels, 80036, Amiens, France

³ Service d Anatomie Pathologique, CHU Nord, Amiens, France

⁴ Laboratoire de Physiologie Animale, Faculté des Sciences, Université Ibn-Zohr, Agadir, Morocco

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BMC Cancer 2008, 8:125 doi:10.1186/1471-2407-8-125

Published: 2 May 2008

Abstract

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 TRPC7, 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.