Document Detail


Contribution of functional voltage-gated Na+ channel expression to cell behaviors involved in the metastatic cascade in rat prostate cancer: I. Lateral motility.
MedLine Citation:
PMID:  12704658     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Previous work suggested that functional voltage-gated Na(+) channels (VGSCs) are expressed specifically in strongly metastatic cells of rat and human prostate cancer (PCa), thereby raising the possibility that VGSC activity could be involved in cellular behavior(s) related to the metastatic cascade. In the present study, the possible role of VGSCs in the lateral motility of rat PCa cells was investigated in vitro by testing the effect of modulators that either block or enhance VGSC activity. Two rat PCa cell lines of markedly different metastatic ability were used in a comparative approach: the strongly metastatic MAT-LyLu and the weakly metastatic AT-2 cell line, only the former being known to express functional VGSCs. Using both electrophysiological recording and a motility assay, the effects of two VGSC blockers (tetrodotoxin and phenytoin) and four potential openers (veratridine, aconitine, ATX II, and brevetoxin) were monitored on (a) Na(+) channel activity and (b) cell motility over 48 h. Tetrodotoxin (at 1 microM) and phenytoin (at 50 microM) both decreased the motility index of the MAT-LyLu cell line by 47 and 11%, respectively. Veratridine (at 20 microM) and brevetoxin (at 10 nM) had no effect on the motility of either cell line, whilst aconitine (at 100 microM) and ATX II (at 25 pM) significantly increased the motility of the MAT-LyLu cell line by 15 and 9%, respectively. Importantly, at the concentrations used, none of these drugs had effects on the proliferation or viability of either cell line. The results, taken together, would suggest strongly that functional VGSC expression enhances cellular motility of PCa cells. The relevance of these findings to the metastatic process in PCa is discussed.
Authors:
S P Fraser; V Salvador; E A Manning; J Mizal; S Altun; M Raza; R J Berridge; M B A Djamgoz
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of cellular physiology     Volume:  195     ISSN:  0021-9541     ISO Abbreviation:  J. Cell. Physiol.     Publication Date:  2003 Jun 
Date Detail:
Created Date:  2003-04-21     Completed Date:  2003-05-27     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0050222     Medline TA:  J Cell Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  479-87     Citation Subset:  IM    
Copyright Information:
Copyright 2003 Wiley-Liss, Inc.
Affiliation:
Imperial College of Science, Technology, and Medicine, Department of Biological Sciences, Sir Alexander Fleming Building, Imperial College Road, London, United Kingdom. s.p.fraser@ic.ac.uk
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MeSH Terms
Descriptor/Qualifier:
Aconitine / pharmacology
Animals
Carcinoma / metabolism,  pathology,  physiopathology
Cell Division
Cell Movement*
Cnidarian Venoms / pharmacology
Cytoskeletal Proteins / physiology
Cytoskeleton / physiology
Gene Expression Regulation, Neoplastic
Ion Transport
Male
Marine Toxins / pharmacology
Neoplasm Metastasis
Oxocins / pharmacology
Patch-Clamp Techniques
Phenytoin / pharmacology
Prostatic Neoplasms / metabolism,  pathology,  physiopathology*
Rats
Sodium Channel Blockers / pharmacology
Sodium Channels / metabolism,  physiology*
Tetrodotoxin / pharmacology
Tumor Cells, Cultured
Veratridine / pharmacology
Chemical
Reg. No./Substance:
0/Cnidarian Venoms; 0/Cytoskeletal Proteins; 0/Marine Toxins; 0/Oxocins; 0/Sodium Channel Blockers; 0/Sodium Channels; 302-27-2/Aconitine; 4368-28-9/Tetrodotoxin; 57-41-0/Phenytoin; 60748-45-0/toxin II (Anemonia sulcata); 71-62-5/Veratridine; 98225-48-0/brevetoxin

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


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