| Contribution of functional voltage-gated Na+ channel expression to cell behaviors involved in the metastatic cascade in rat prostate cancer: I. Lateral motility. | |
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MedLine Citation:
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PMID: 12704658 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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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:
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Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Journal of cellular physiology Volume: 195 ISSN: 0021-9541 ISO Abbreviation: J. Cell. Physiol. Publication Date: 2003 Jun |
Date Detail:
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Created Date: 2003-04-21 Completed Date: 2003-05-27 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0050222 Medline TA: J Cell Physiol Country: United States |
Other Details:
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Languages: eng Pagination: 479-87 Citation Subset: IM |
Copyright Information:
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Copyright 2003 Wiley-Liss, Inc. |
Affiliation:
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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 |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Aconitine
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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:
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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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