However, the molecular nature of those K+ channels implicated in prostate cancer cell proliferation and the mechanisms through which they control proliferation are still unknown.
Also, TRPM8 was suggested to act as a "Ca2+ release channel" on stores in prostate carcinoma cell lines [39].
Several studies have confirmed the increased expression of T-type Cav3.2 channels in breast, colon, prostate, ovarian, esophageal, and colon cancers and in glioblastoma, hepatoma, and melanoma [ 20].
These results highlight that there is a functional coupling in LNCaP cells between BK channels and Cav3.2 channels and that this coupling may participate in prostate cancer cell growth.
More recently, it was shown that 2-APB is an efficient inhibitor of the epithelial calcium channel TRPV6 which is overexpressed in prostate cancer.
In addition, a variety of tumor cells, which include the hERG potassium channel proteins, are also present in prostate cancer cells with high expression [ 3].
Finally, using specific inhibitors and siRNA, we show that BK and Cav3.2 channels set the resting membrane potential in prostate cancer cells and thereby participate in cell proliferation.
The membrane hyperpolarization likely was produced by activation of potassium channels, which are present at high density in prostate cancer cells [ 21].
Several genes in TRPV channel have been detected to be up-regulated in prostate, colon, and breast cancer cells [ 40- 42].
Therefore, TRPM8 channels can be considered as a valuable prognostic marker in prostate cancer [ 23].
