Initial steps of metastasis: Cell invasion and endothelial transmigration

Metastasis is the leading cause of cancer mortality. The metastatic cascade represents a multi-step process which includes local tumor cell invasion, entry into the vasculature followed by the exit of carcinoma cells from the circulation and colonization at the distal sites. At the earliest stage of...

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Autores principales: van Zijl, Franziska, Krupitza, Georg, Mikulits, Wolfgang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4028085/
https://www.ncbi.nlm.nih.gov/pubmed/21605699
http://dx.doi.org/10.1016/j.mrrev.2011.05.002
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author van Zijl, Franziska
Krupitza, Georg
Mikulits, Wolfgang
author_facet van Zijl, Franziska
Krupitza, Georg
Mikulits, Wolfgang
author_sort van Zijl, Franziska
collection PubMed
description Metastasis is the leading cause of cancer mortality. The metastatic cascade represents a multi-step process which includes local tumor cell invasion, entry into the vasculature followed by the exit of carcinoma cells from the circulation and colonization at the distal sites. At the earliest stage of successful cancer cell dissemination, the primary cancer adapts the secondary site of tumor colonization involving the tumor–stroma crosstalk. The migration and plasticity of cancer cells as well as the surrounding environment such as stromal and endothelial cells are mandatory. Consequently, the mechanisms of cell movement are of utmost relevance for targeted intervention of which three different types have been reported. Tumor cells can migrate either collectively, in a mesenchymal or in an amoeboid type of movement and intravasate the blood or lymph vasculature. Intravasation by the interaction of tumor cells with the vascular endothelium is mechanistically poorly understood. Changes in the epithelial plasticity enable carcinoma cells to switch between these types of motility. The types of migration may change depending on the intervention thereby increasing the velocity and aggressiveness of invading cancer cells. Interference with collective or mesenchymal cell invasion by targeting integrin expression or metalloproteinase activity, respectively, resulted in an amoeboid cell phenotype as the ultimate exit strategy of cancer cells. There are little mechanistic details reported in vivo showing that the amoeboid behavior can be either reversed or efficiently inhibited. Future concepts of metastasis intervention must simultaneously address the collective, mesenchymal and amoeboid mechanisms of cell invasion in order to advance in anti-metastatic strategies as these different types of movement can coexist and cooperate. Beyond the targeting of cell movements, the adhesion of cancer cells to the stroma in heterotypic circulating tumor cell emboli is of paramount relevance for anti-metastatic therapy.
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spelling pubmed-40280852014-05-28 Initial steps of metastasis: Cell invasion and endothelial transmigration van Zijl, Franziska Krupitza, Georg Mikulits, Wolfgang Mutat Res Review Metastasis is the leading cause of cancer mortality. The metastatic cascade represents a multi-step process which includes local tumor cell invasion, entry into the vasculature followed by the exit of carcinoma cells from the circulation and colonization at the distal sites. At the earliest stage of successful cancer cell dissemination, the primary cancer adapts the secondary site of tumor colonization involving the tumor–stroma crosstalk. The migration and plasticity of cancer cells as well as the surrounding environment such as stromal and endothelial cells are mandatory. Consequently, the mechanisms of cell movement are of utmost relevance for targeted intervention of which three different types have been reported. Tumor cells can migrate either collectively, in a mesenchymal or in an amoeboid type of movement and intravasate the blood or lymph vasculature. Intravasation by the interaction of tumor cells with the vascular endothelium is mechanistically poorly understood. Changes in the epithelial plasticity enable carcinoma cells to switch between these types of motility. The types of migration may change depending on the intervention thereby increasing the velocity and aggressiveness of invading cancer cells. Interference with collective or mesenchymal cell invasion by targeting integrin expression or metalloproteinase activity, respectively, resulted in an amoeboid cell phenotype as the ultimate exit strategy of cancer cells. There are little mechanistic details reported in vivo showing that the amoeboid behavior can be either reversed or efficiently inhibited. Future concepts of metastasis intervention must simultaneously address the collective, mesenchymal and amoeboid mechanisms of cell invasion in order to advance in anti-metastatic strategies as these different types of movement can coexist and cooperate. Beyond the targeting of cell movements, the adhesion of cancer cells to the stroma in heterotypic circulating tumor cell emboli is of paramount relevance for anti-metastatic therapy. Elsevier 2011-07 /pmc/articles/PMC4028085/ /pubmed/21605699 http://dx.doi.org/10.1016/j.mrrev.2011.05.002 Text en © 2011 Elsevier B.V. All rights reserved. https://creativecommons.org/licenses/by-nc-nd/3.0/ Open Access under CC BY-NC-ND 3.0 (https://creativecommons.org/licenses/by-nc-nd/3.0/) license
spellingShingle Review
van Zijl, Franziska
Krupitza, Georg
Mikulits, Wolfgang
Initial steps of metastasis: Cell invasion and endothelial transmigration
title Initial steps of metastasis: Cell invasion and endothelial transmigration
title_full Initial steps of metastasis: Cell invasion and endothelial transmigration
title_fullStr Initial steps of metastasis: Cell invasion and endothelial transmigration
title_full_unstemmed Initial steps of metastasis: Cell invasion and endothelial transmigration
title_short Initial steps of metastasis: Cell invasion and endothelial transmigration
title_sort initial steps of metastasis: cell invasion and endothelial transmigration
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4028085/
https://www.ncbi.nlm.nih.gov/pubmed/21605699
http://dx.doi.org/10.1016/j.mrrev.2011.05.002
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