Research

We are interested in the alterations of ion channel electrophysiological properties and molecular biology during prostate tumorigenesis. Prostate cancer is the most common non-cutaneous human malignancy and the second most lethal tumour among men, with the highest incidence in industrialized countries. Understanding the processes leading to prostate cancers and developing new therapeutic targets are necessary to improve both the survival and the every day life of patients. Until recently, the molecular nature and the regulation of ion channels involved in the prostate carcinogenesis and cancer evolution towards androgen independence remain poorly understood.

Our work over previous years has allowed us to identify various ion channels expressed in normal or cancerous prostate cells which take a significant part in the prostate’s pathophysiology (apoptosis, proliferation and cellular differentiation). According to these results, ion channels determining the calcium signature would appear to us to be the best potential candidates as tumour markers and pharmacological targets (Cancer Res. 2006; Oncogene 2007; J. Clin. Invest. 2007). Following this identification stage, we are now concentrating our research, on the mechanisms of the regulation/modulation of several most promising channels (channels from Transient Receptor Potential (TRP) family: TRPV6, TRPV2, TRPM8; Store Operated Channels (SOC) and voltage dependent CaV3.2 calcium channels). Indeed, the aberration of these mechanisms could lead to the development of the pathophysiological processes associated with prostate cancer. We are therefore studying how these channels are remodelled in tumour cells and the significance this has for the maintenance of the cancer phenotype. In addition, we are focusing our efforts on the molecular targeting of the channels for the elaboration of effective therapies and on the developing of animal models allowing to check the physiological role of these channels in normal and cancerous prostate.