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Cancer cells with trapped nuclei cut their way through the extracellular matrix
When an invading cancer cell attempts to pass through a hole in the extracellular matrix (ECM) which is too small for its nucleus, this generates physical tension. This tension is sensed by a nucleus–centrosome connection that activates trafficking of endosomal vesicles containing the matrix metallo...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6160491/ https://www.ncbi.nlm.nih.gov/pubmed/30262828 http://dx.doi.org/10.1038/s41467-018-06351-6 |
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author | Dornier, Emmanuel Norman, Jim C. |
author_facet | Dornier, Emmanuel Norman, Jim C. |
author_sort | Dornier, Emmanuel |
collection | PubMed |
description | When an invading cancer cell attempts to pass through a hole in the extracellular matrix (ECM) which is too small for its nucleus, this generates physical tension. This tension is sensed by a nucleus–centrosome connection that activates trafficking of endosomal vesicles containing the matrix metalloprotease, MT1-MMP1 to the site of constraint. Recent evidence shows how focussed ECM degradation relieves the constraint and allows cancer cells to continue invading. |
format | Online Article Text |
id | pubmed-6160491 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-61604912018-10-01 Cancer cells with trapped nuclei cut their way through the extracellular matrix Dornier, Emmanuel Norman, Jim C. Nat Commun Comment When an invading cancer cell attempts to pass through a hole in the extracellular matrix (ECM) which is too small for its nucleus, this generates physical tension. This tension is sensed by a nucleus–centrosome connection that activates trafficking of endosomal vesicles containing the matrix metalloprotease, MT1-MMP1 to the site of constraint. Recent evidence shows how focussed ECM degradation relieves the constraint and allows cancer cells to continue invading. Nature Publishing Group UK 2018-09-27 /pmc/articles/PMC6160491/ /pubmed/30262828 http://dx.doi.org/10.1038/s41467-018-06351-6 Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Comment Dornier, Emmanuel Norman, Jim C. Cancer cells with trapped nuclei cut their way through the extracellular matrix |
title | Cancer cells with trapped nuclei cut their way through the extracellular matrix |
title_full | Cancer cells with trapped nuclei cut their way through the extracellular matrix |
title_fullStr | Cancer cells with trapped nuclei cut their way through the extracellular matrix |
title_full_unstemmed | Cancer cells with trapped nuclei cut their way through the extracellular matrix |
title_short | Cancer cells with trapped nuclei cut their way through the extracellular matrix |
title_sort | cancer cells with trapped nuclei cut their way through the extracellular matrix |
topic | Comment |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6160491/ https://www.ncbi.nlm.nih.gov/pubmed/30262828 http://dx.doi.org/10.1038/s41467-018-06351-6 |
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