The mechanics of metastasis: insights from a computational model.

Although it may seem obvious that mechanical forces are required to drive metastatic cell movements, understanding of the mechanical aspects of metastasis has lagged far behind genetic and biochemical knowledge. The goal of this study is to learn about the mechanics of metastasis using a cell-based...

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Autores principales:	G Wayne Brodland, Jim H Veldhuis
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/bbb749e55f76477ab02213bbf8ae8085
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spelling	oai:doaj.org-article:bbb749e55f76477ab02213bbf8ae80852021-11-18T07:04:08ZThe mechanics of metastasis: insights from a computational model.1932-620310.1371/journal.pone.0044281https://doaj.org/article/bbb749e55f76477ab02213bbf8ae80852012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23028513/?tool=EBIhttps://doaj.org/toc/1932-6203Although it may seem obvious that mechanical forces are required to drive metastatic cell movements, understanding of the mechanical aspects of metastasis has lagged far behind genetic and biochemical knowledge. The goal of this study is to learn about the mechanics of metastasis using a cell-based finite element model that proved useful for advancing knowledge about the forces that drive embryonic cell and tissue movements. Metastasis, the predominant cause of cancer-related deaths, involves a series of mechanical events in which one or more cells dissociate from a primary tumour, migrate through normal tissue, traverse in and out of a multi-layer circulatory system vessel and resettle. The present work focuses on the dissemination steps, from dissociation to circulation. The model shows that certain surface tension relationships must be satisfied for cancerous cells to dissociate from a primary tumour and that these equations are analogous to those that govern dissociation of embryonic cells. For a dissociated cell to then migrate by invadopodium extension and contraction and exhibit the shapes seen in experiments, the invadopodium must generate a contraction equal to approximately twice that produced by the interfacial tension associated with surrounding cells. Intravasation through the wall of a vessel is governed by relationships akin to those in the previous two steps, while release from the vessel wall is governed by equations that involve surface and interfacial tensions. The model raises a number of potential research questions. It also identifies how specific mechanical properties and the sub-cellular structural components that give rise to them might be changed so as to thwart particular metastatic steps and thereby block the spread of cancer.G Wayne BrodlandJim H VeldhuisPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 9, p e44281 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q G Wayne Brodland Jim H Veldhuis The mechanics of metastasis: insights from a computational model.
description	Although it may seem obvious that mechanical forces are required to drive metastatic cell movements, understanding of the mechanical aspects of metastasis has lagged far behind genetic and biochemical knowledge. The goal of this study is to learn about the mechanics of metastasis using a cell-based finite element model that proved useful for advancing knowledge about the forces that drive embryonic cell and tissue movements. Metastasis, the predominant cause of cancer-related deaths, involves a series of mechanical events in which one or more cells dissociate from a primary tumour, migrate through normal tissue, traverse in and out of a multi-layer circulatory system vessel and resettle. The present work focuses on the dissemination steps, from dissociation to circulation. The model shows that certain surface tension relationships must be satisfied for cancerous cells to dissociate from a primary tumour and that these equations are analogous to those that govern dissociation of embryonic cells. For a dissociated cell to then migrate by invadopodium extension and contraction and exhibit the shapes seen in experiments, the invadopodium must generate a contraction equal to approximately twice that produced by the interfacial tension associated with surrounding cells. Intravasation through the wall of a vessel is governed by relationships akin to those in the previous two steps, while release from the vessel wall is governed by equations that involve surface and interfacial tensions. The model raises a number of potential research questions. It also identifies how specific mechanical properties and the sub-cellular structural components that give rise to them might be changed so as to thwart particular metastatic steps and thereby block the spread of cancer.
format	article
author	G Wayne Brodland Jim H Veldhuis
author_facet	G Wayne Brodland Jim H Veldhuis
author_sort	G Wayne Brodland
title	The mechanics of metastasis: insights from a computational model.
title_short	The mechanics of metastasis: insights from a computational model.
title_full	The mechanics of metastasis: insights from a computational model.
title_fullStr	The mechanics of metastasis: insights from a computational model.
title_full_unstemmed	The mechanics of metastasis: insights from a computational model.
title_sort	mechanics of metastasis: insights from a computational model.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/bbb749e55f76477ab02213bbf8ae8085
work_keys_str_mv	AT gwaynebrodland themechanicsofmetastasisinsightsfromacomputationalmodel AT jimhveldhuis themechanicsofmetastasisinsightsfromacomputationalmodel AT gwaynebrodland mechanicsofmetastasisinsightsfromacomputationalmodel AT jimhveldhuis mechanicsofmetastasisinsightsfromacomputationalmodel
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The mechanics of metastasis: insights from a computational model.

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