Open AccessIntermediate-conductance Ca2+-activated K+ channels (IKCa1) regulate human prostate cancer cell proliferation through a close control of calcium entry
Author(s) -
Hélène Lallet-Daher,
Morad Roudbaraki,
Alexis Bavencoffe,
Pascal Mariot,
Florian Gackière,
Gabriel Bidaux,
Rémi Urbain,
Pierre Gosset,
Philippe Delcourt,
Laurence Fleurisse,
Christian Slomianny,
Etienne Dewailly,
Brigitte Mauroy,
J Bonnal,
Roman Skryma,
Natalia Prevarskaya
Publication year - 2009
Publication title -
oncogene
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.395
H-Index - 342
eISSN - 1476-5594
pISSN - 0950-9232
DOI - 10.1038/onc.2009.25
Subject(s) - biology , cell growth , carcinogenesis , calcium , microbiology and biotechnology , potassium channel , voltage dependent calcium channel , t type calcium channel , prostate cancer , cell , calcium channel , calcium signaling , signal transduction , endocrinology , cancer , medicine , biochemistry , gene , genetics
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.