Document Detail


The motility of glioblastoma tumour cells is modulated by intracellular cofilin expression in a concentration-dependent manner.
MedLine Citation:
PMID:  15662725     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The invasive behaviour of tumour cells has been attributed in part to dysregulated cell motility. Members of the ADF/Cofilin family of actin-binding proteins are known to increase microfilament dynamics by increasing the rate at which actin monomers leave the pointed end of the filament and by a filament-severing activity. As depolymerisation is a rate-limiting step in actin dynamics, ADF/Cofilins are suspected to facilitate the motility of cells. To test this, we investigated the influence of cofilin on tumour motility by transient and stably overexpressing cofilin in the human glioblastoma cell line, U373 MG. Several different methods were used to ascertain the level of cofilin in overexpressing clones and this was correlated with their rate of random locomotion. A biphasic relationship between cofilin level and locomotory rate was found. Clones that displayed a moderate amount of overproduction of cofilin were found to have increased rates of locomotion approximately linear to the overproduction of cofilin up to an optimal cofilin level of about 4.5 times that of wild type cells at which the cells were almost twice as fast. However, clones producing more than this optimal amount were found to locomote at progressively reduced speeds. Cells that overexpress cofilin have reduced stress fibres compared to control cells showing that the excess cofilin affects the actin cytoskeleton. We conclude that overexpression of cofilin enhances the motility of glioblastoma tumour cells in a concentration-dependent fashion, which is likely to contribute to their invasiveness.
Authors:
Celestial T Yap; T Ian Simpson; Thomas Pratt; David J Price; Sutherland K Maciver
Related Documents :
22399585 - Stem-like cells in bladder cancer cell lines with differential sensitivity to cisplatin.
561095 - Computer evidence concerning the chemotactic signal in dictyostelium discoideum.
10506935 - Cohort migration of carcinoma cells: differentiated colorectal carcinoma cells move as ...
15153605 - Controlled, scalable embryonic stem cell differentiation culture.
24859355 - Sodium arsenite induces ros-dependent autophagic cell death in pancreatic β-cells.
23692085 - In vitro cytotoxicity of gymnema montanum in human leukaemia hl-60 cells; induction of ...
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Cell motility and the cytoskeleton     Volume:  60     ISSN:  0886-1544     ISO Abbreviation:  Cell Motil. Cytoskeleton     Publication Date:  2005 Mar 
Date Detail:
Created Date:  2005-02-15     Completed Date:  2005-06-10     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8605339     Medline TA:  Cell Motil Cytoskeleton     Country:  United States    
Other Details:
Languages:  eng     Pagination:  153-65     Citation Subset:  IM    
Copyright Information:
Copyright 2005 Wiley-Liss, Inc.
Affiliation:
Genes and Development Group, School of Biomedical and Clinical Laboratory Sciences, College of Medicine, University of Edinburgh, Scotland, United Kingdom.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Actin Depolymerizing Factors
Cell Line, Tumor
Cell Movement / physiology*
Fluorescent Antibody Technique
Gene Expression Regulation
Glioblastoma / metabolism*,  ultrastructure
Green Fluorescent Proteins / biosynthesis
Humans
Microfilament Proteins / biosynthesis*
Microscopy, Confocal
Plasmids / genetics
Transfection
Chemical
Reg. No./Substance:
0/Actin Depolymerizing Factors; 0/Microfilament Proteins; 0/enhanced green fluorescent protein; 147336-22-9/Green Fluorescent Proteins

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


Previous Document:  Haplotype sharing transmission/disequilibrium tests that allow for genotyping errors.
Next Document:  Calcium transients regulate titin organization during myofibrillogenesis.