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Glioblastoma motility occurs in the absence of actin polymer
In fibroblasts and keratocytes, motility is actin dependent, while microtubules play a secondary role, providing directional guidance. We demonstrate here that the motility of glioblastoma cells is exceptional, in that it occurs in cells depleted of assembled actin. Cells display persistent motility...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The American Society for Cell Biology
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3128524/ https://www.ncbi.nlm.nih.gov/pubmed/21551075 http://dx.doi.org/10.1091/mbc.E10-10-0849 |
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author | Panopoulos, Andreas Howell, Michael Fotedar, Rati Margolis, Robert L. |
author_facet | Panopoulos, Andreas Howell, Michael Fotedar, Rati Margolis, Robert L. |
author_sort | Panopoulos, Andreas |
collection | PubMed |
description | In fibroblasts and keratocytes, motility is actin dependent, while microtubules play a secondary role, providing directional guidance. We demonstrate here that the motility of glioblastoma cells is exceptional, in that it occurs in cells depleted of assembled actin. Cells display persistent motility in the presence of actin inhibitors at concentrations sufficient to fully disassemble actin. Such actin independent motility is characterized by the extension of cell protrusions containing abundant microtubule polymers. Strikingly, glioblastoma cells exhibit no motility in the presence of microtubule inhibitors, at concentrations that disassemble labile microtubule polymers. In accord with an unconventional mode of motility, glioblastoma cells have some unusual requirements for the Rho GTPases. While Rac1 is required for lamellipodial protrusions in fibroblasts, expression of dominant negative Rac1 does not suppress glioblastoma migration. Other GTPase mutants are largely without unique effect, except dominant positive Rac1-Q61L, and rapidly cycling Rac1-F28L, which substantially suppress glioblastoma motility. We conclude that glioblastoma cells display an unprecedented mode of intrinsic motility that can occur in the absence of actin polymer, and that appears to require polymerized microtubules. |
format | Online Article Text |
id | pubmed-3128524 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | The American Society for Cell Biology |
record_format | MEDLINE/PubMed |
spelling | pubmed-31285242011-09-16 Glioblastoma motility occurs in the absence of actin polymer Panopoulos, Andreas Howell, Michael Fotedar, Rati Margolis, Robert L. Mol Biol Cell Articles In fibroblasts and keratocytes, motility is actin dependent, while microtubules play a secondary role, providing directional guidance. We demonstrate here that the motility of glioblastoma cells is exceptional, in that it occurs in cells depleted of assembled actin. Cells display persistent motility in the presence of actin inhibitors at concentrations sufficient to fully disassemble actin. Such actin independent motility is characterized by the extension of cell protrusions containing abundant microtubule polymers. Strikingly, glioblastoma cells exhibit no motility in the presence of microtubule inhibitors, at concentrations that disassemble labile microtubule polymers. In accord with an unconventional mode of motility, glioblastoma cells have some unusual requirements for the Rho GTPases. While Rac1 is required for lamellipodial protrusions in fibroblasts, expression of dominant negative Rac1 does not suppress glioblastoma migration. Other GTPase mutants are largely without unique effect, except dominant positive Rac1-Q61L, and rapidly cycling Rac1-F28L, which substantially suppress glioblastoma motility. We conclude that glioblastoma cells display an unprecedented mode of intrinsic motility that can occur in the absence of actin polymer, and that appears to require polymerized microtubules. The American Society for Cell Biology 2011-07-01 /pmc/articles/PMC3128524/ /pubmed/21551075 http://dx.doi.org/10.1091/mbc.E10-10-0849 Text en © 2011 Panopoulos et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0). “ASCB®,” “The American Society for Cell Biology®,” and “Molecular Biology of the Cell®” are registered trademarks of The American Society of Cell Biology. |
spellingShingle | Articles Panopoulos, Andreas Howell, Michael Fotedar, Rati Margolis, Robert L. Glioblastoma motility occurs in the absence of actin polymer |
title | Glioblastoma motility occurs in the absence of actin polymer |
title_full | Glioblastoma motility occurs in the absence of actin polymer |
title_fullStr | Glioblastoma motility occurs in the absence of actin polymer |
title_full_unstemmed | Glioblastoma motility occurs in the absence of actin polymer |
title_short | Glioblastoma motility occurs in the absence of actin polymer |
title_sort | glioblastoma motility occurs in the absence of actin polymer |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3128524/ https://www.ncbi.nlm.nih.gov/pubmed/21551075 http://dx.doi.org/10.1091/mbc.E10-10-0849 |
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