Overcoming EMT-driven therapeutic resistance by BH3 mimetics

Epithelial-mesenchymal transition (EMT) contributes to the progression of cancer through enhanced invasion and stem-like properties of cancer cells. Additionally, EMT confers resistance towards many chemotherapeutics. We recently described a mechanism that mediates EMT-driven chemoresistance through...

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Detalles Bibliográficos
Autores principales: Keitel, Ulrike, Scheel, Christina, Dobbelstein, Matthias
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2014
Materias:
Research Perspective
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4278270/
https://www.ncbi.nlm.nih.gov/pubmed/25593997
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author Keitel, Ulrike
Scheel, Christina
Dobbelstein, Matthias
author_facet Keitel, Ulrike
Scheel, Christina
Dobbelstein, Matthias
author_sort Keitel, Ulrike
collection PubMed
description Epithelial-mesenchymal transition (EMT) contributes to the progression of cancer through enhanced invasion and stem-like properties of cancer cells. Additionally, EMT confers resistance towards many chemotherapeutics. We recently described a mechanism that mediates EMT-driven chemoresistance through augmented levels of Bcl-xL, an anti-apoptotic member of the Bcl-2 family (Keitel et al., Oncotarget, in press). Here, we elaborate on how these findings pertain to cancer cells dispersed in the tumor-adjacent stroma of breast cancer tissues, and how BH3-mimetics may provide a therapeutic strategy to eliminate cancer cell populations that have passed through an EMT.
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spelling pubmed-42782702015-01-15 Overcoming EMT-driven therapeutic resistance by BH3 mimetics Keitel, Ulrike Scheel, Christina Dobbelstein, Matthias Oncoscience Research Perspective Epithelial-mesenchymal transition (EMT) contributes to the progression of cancer through enhanced invasion and stem-like properties of cancer cells. Additionally, EMT confers resistance towards many chemotherapeutics. We recently described a mechanism that mediates EMT-driven chemoresistance through augmented levels of Bcl-xL, an anti-apoptotic member of the Bcl-2 family (Keitel et al., Oncotarget, in press). Here, we elaborate on how these findings pertain to cancer cells dispersed in the tumor-adjacent stroma of breast cancer tissues, and how BH3-mimetics may provide a therapeutic strategy to eliminate cancer cell populations that have passed through an EMT. Impact Journals LLC 2014-11-05 /pmc/articles/PMC4278270/ /pubmed/25593997 Text en © 2014 Keitel et al. http://creativecommons.org/licenses/by/2.5/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Perspective
Keitel, Ulrike
Scheel, Christina
Dobbelstein, Matthias
Overcoming EMT-driven therapeutic resistance by BH3 mimetics
title Overcoming EMT-driven therapeutic resistance by BH3 mimetics
title_full Overcoming EMT-driven therapeutic resistance by BH3 mimetics
title_fullStr Overcoming EMT-driven therapeutic resistance by BH3 mimetics
title_full_unstemmed Overcoming EMT-driven therapeutic resistance by BH3 mimetics
title_short Overcoming EMT-driven therapeutic resistance by BH3 mimetics
title_sort overcoming emt-driven therapeutic resistance by bh3 mimetics
topic Research Perspective
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4278270/
https://www.ncbi.nlm.nih.gov/pubmed/25593997
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