Document Detail


Functional and molecular identification of intermediate-conductance Ca(2+)-activated K(+) channels in breast cancer cells: association with cell cycle progression.
MedLine Citation:
PMID:  14985237     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We have previously reported that the hEAG K(+) channels are responsible for the potential membrane hyperpolarization that induces human breast cancer cell progression into the G1 phase of the cell cycle. In the present study, we evaluate the role and functional expression of the intermediate-conductance Ca(2+)-activated K(+) channel, hIK1-like, in controlling cell cycle progression. Our results demonstrate that hIK1 current density increased in cells synchronized at the end of the G1 or S phase compared with those in the early G1 phase. This increased current density paralleled the enhancement in hIK1 mRNA levels and the highly negative membrane potential. Furthermore, in cells synchronized at the end of G1 or S phases, basal cytosolic Ca(2+) concentration ([Ca(2+)](i)) was also higher than in cells arrested in early G1. Blocking hIK1 channels with a specific blocker, clotrimazole, induced both membrane potential depolarization and a decrease in the [Ca(2+)](i) in cells arrested at the end of G1 and S phases but not in cells arrested early in the G1 phase. Blocking hIK1 with clotrimazole also induced cell proliferation inhibition but to a lesser degree than blocking hEAG with astemizole. The two drugs were essentially additive, inhibiting MCF-7 cell proliferation by 82% and arresting >90% of cells in the G1 phase. Thus, although the progression of MCF-7 cells through the early G1 phase is dependent on the activation of hEAG K(+) channels, when it comes to G1 and checkpoint G1/S transition, the membrane potential appears to be primarily dependent on the hIK1-activity level.
Authors:
Halima Ouadid-Ahidouch; Morad Roudbaraki; Philippe Delcourt; Ahmed Ahidouch; Nathalie Joury; Natalia Prevarskaya
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2004-02-25
Journal Detail:
Title:  American journal of physiology. Cell physiology     Volume:  287     ISSN:  0363-6143     ISO Abbreviation:  Am. J. Physiol., Cell Physiol.     Publication Date:  2004 Jul 
Date Detail:
Created Date:  2004-06-10     Completed Date:  2004-07-23     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  100901225     Medline TA:  Am J Physiol Cell Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  C125-34     Citation Subset:  IM    
Affiliation:
Laboratoire de Physiologie Cellulaire, Université des Sciences et Technologies de Lille, Cedex, France. ha-sciences@u-picardie.fr
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MeSH Terms
Descriptor/Qualifier:
Breast Neoplasms / metabolism,  pathology*,  physiopathology*
Calcium / metabolism,  pharmacology
Cell Cycle*
Cell Division / drug effects
Cell Line, Tumor
Cytosol / metabolism
Ether-A-Go-Go Potassium Channels
Female
G1 Phase
Humans
Intermediate-Conductance Calcium-Activated Potassium Channels
Membrane Potentials
Osmolar Concentration
Potassium Channel Blockers / pharmacology
Potassium Channels / drug effects,  genetics,  metabolism*
Potassium Channels, Calcium-Activated*
RNA, Messenger / metabolism
Chemical
Reg. No./Substance:
0/Ether-A-Go-Go Potassium Channels; 0/Intermediate-Conductance Calcium-Activated Potassium Channels; 0/KCNN4 protein, human; 0/Potassium Channel Blockers; 0/Potassium Channels; 0/Potassium Channels, Calcium-Activated; 0/RNA, Messenger; 7440-70-2/Calcium

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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