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Integrin Signaling in Cancer Cell Survival and Chemoresistance

Resistance to apoptosis and chemotherapy is a hallmark of cancer cells, and it is a critical factor in cancer recurrence and patient relapse. Extracellular matrix (ECM) via its receptors, the integrins, has emerged as a major pathway contributing to cancer cell survival and resistance to chemotherap...

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Detalles Bibliográficos
Autores principales: Aoudjit, Fawzi, Vuori, Kristiina
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3332161/
https://www.ncbi.nlm.nih.gov/pubmed/22567280
http://dx.doi.org/10.1155/2012/283181
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author Aoudjit, Fawzi
Vuori, Kristiina
author_facet Aoudjit, Fawzi
Vuori, Kristiina
author_sort Aoudjit, Fawzi
collection PubMed
description Resistance to apoptosis and chemotherapy is a hallmark of cancer cells, and it is a critical factor in cancer recurrence and patient relapse. Extracellular matrix (ECM) via its receptors, the integrins, has emerged as a major pathway contributing to cancer cell survival and resistance to chemotherapy. Several studies over the last decade have demonstrated that ECM/integrin signaling provides a survival advantage to various cancer cell types against numerous chemotherapeutic drugs and against antibody therapy. In this paper, we will discuss the major findings on how ECM/integrin signaling protects tumor cells from drug-induced apoptosis. We will also discuss the potential role of ECM in malignant T-cell survival and in cancer stem cell resistance. Understanding how integrins and their signaling partners promote tumor cell survival and chemoresistance will likely lead to the development of new therapeutic strategies and agents for cancer treatment.
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spelling pubmed-33321612012-05-07 Integrin Signaling in Cancer Cell Survival and Chemoresistance Aoudjit, Fawzi Vuori, Kristiina Chemother Res Pract Review Article Resistance to apoptosis and chemotherapy is a hallmark of cancer cells, and it is a critical factor in cancer recurrence and patient relapse. Extracellular matrix (ECM) via its receptors, the integrins, has emerged as a major pathway contributing to cancer cell survival and resistance to chemotherapy. Several studies over the last decade have demonstrated that ECM/integrin signaling provides a survival advantage to various cancer cell types against numerous chemotherapeutic drugs and against antibody therapy. In this paper, we will discuss the major findings on how ECM/integrin signaling protects tumor cells from drug-induced apoptosis. We will also discuss the potential role of ECM in malignant T-cell survival and in cancer stem cell resistance. Understanding how integrins and their signaling partners promote tumor cell survival and chemoresistance will likely lead to the development of new therapeutic strategies and agents for cancer treatment. Hindawi Publishing Corporation 2012 2012-04-11 /pmc/articles/PMC3332161/ /pubmed/22567280 http://dx.doi.org/10.1155/2012/283181 Text en Copyright © 2012 F. Aoudjit and K. Vuori. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Aoudjit, Fawzi
Vuori, Kristiina
Integrin Signaling in Cancer Cell Survival and Chemoresistance
title Integrin Signaling in Cancer Cell Survival and Chemoresistance
title_full Integrin Signaling in Cancer Cell Survival and Chemoresistance
title_fullStr Integrin Signaling in Cancer Cell Survival and Chemoresistance
title_full_unstemmed Integrin Signaling in Cancer Cell Survival and Chemoresistance
title_short Integrin Signaling in Cancer Cell Survival and Chemoresistance
title_sort integrin signaling in cancer cell survival and chemoresistance
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3332161/
https://www.ncbi.nlm.nih.gov/pubmed/22567280
http://dx.doi.org/10.1155/2012/283181
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