Abstract
Accumulating data point to K(+) channels as relevant players in controlling cell cycle progression and proliferation of human cancer cells, including prostate cancer (PCa) cells. However, the mechanism(s) by which K(+) channels control PCa cell proliferation remain illusive. In this study, using the techniques of molecular biology, biochemistry, electrophysiology and calcium imaging, we studied the expression and functionality of intermediate-conductance calcium-activated potassium channels (IK(Ca1)) in human PCa as well as their involvement in cell proliferation. We showed that IK(Ca1) mRNA and protein were preferentially expressed in human PCa tissues, and inhibition of the IK(Ca1) potassium channel suppressed PCa cell proliferation. The activation of IK(Ca1) hyperpolarizes membrane potential and, by promoting the driving force for calcium, induces calcium entry through TRPV6, a cation channel of the TRP (Transient Receptor Potential) family. Thus, the overexpression of the IK(Ca1) channel is likely to promote carcinogenesis in human prostate tissue.
Highlights
Prostate cancer (PCa) is a leading cause of cancerrelated deaths in western countries (Woolf, 1995)
This study reports on the expression, functionality and involvement in proliferation of the IKCa1 potassium channel in human PCa cells
We showed the essential upregulation of IKCa1 expression in human PCa vs nonPCa tissues and showed that this channel was functional in PCa cell lines as well as primary cultured human PCa epithelial (hPCE) cells
Summary
Prostate cancer (PCa) is a leading cause of cancerrelated deaths in western countries (Woolf, 1995). Ca2 þ-dependent potassium channels (KCa) are involved in cancer-related mechanisms and are attracting increasing attention (Ghanshani et al, 2000; Ouadid-Ahidouch et al, 2001). Intermediate-conductance Ca2 þ -activated K þ channels, IKCa1 ( called IK1, SK4, hSK4, hKCa4 and KCa3.1), are of particular interest, as their expression has been shown to increase in activated T lymphocytes (Ghanshani et al, 2000) and pancreatic cancer cells (Jager et al, 2004) and undergo modulation during the cell cycle in breast cancer cells (Ouadid-Ahidouch et al, 2004). We investigated the expression of IKCa1 in PCa and the mechanism by which it regulates the intracellular calcium concentration and cell proliferation
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