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Molecular Targets of TRAIL-Sensitizing Agents in Colorectal Cancer

Tumor necrosis factor (TNF)-related apoptosis inducing ligand (TRAIL), a member of the TNF superfamily, interacts with its functional death receptors (DRs) and induces apoptosis in a wide range of cancer cell types. Therefore, TRAIL has been considered as an attractive agent for cancer therapy. Howe...

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Detalles Bibliográficos
Autores principales: Stolfi, Carmine, Pallone, Francesco, Monteleone, Giovanni
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Molecular Diversity Preservation International (MDPI) 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3430210/
https://www.ncbi.nlm.nih.gov/pubmed/22942679
http://dx.doi.org/10.3390/ijms13077886
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author Stolfi, Carmine
Pallone, Francesco
Monteleone, Giovanni
author_facet Stolfi, Carmine
Pallone, Francesco
Monteleone, Giovanni
author_sort Stolfi, Carmine
collection PubMed
description Tumor necrosis factor (TNF)-related apoptosis inducing ligand (TRAIL), a member of the TNF superfamily, interacts with its functional death receptors (DRs) and induces apoptosis in a wide range of cancer cell types. Therefore, TRAIL has been considered as an attractive agent for cancer therapy. However, many cancers are resistant to TRAIL-based therapies mainly due to the reduced expression of DRs and/or up-regulation of TRAIL pathway-related anti-apoptotic proteins. Compounds that revert such defects restore the sensitivity of cancer cells to TRAIL, suggesting that combined therapies could help manage neoplastic patients. In this article, we will focus on the TRAIL-sensitizing effects of natural products and synthetic compounds in colorectal cancer (CRC) cells and discuss the molecular mechanisms by which such agents enhance the response of CRC cells to TRAIL.
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spelling pubmed-34302102012-08-31 Molecular Targets of TRAIL-Sensitizing Agents in Colorectal Cancer Stolfi, Carmine Pallone, Francesco Monteleone, Giovanni Int J Mol Sci Review Tumor necrosis factor (TNF)-related apoptosis inducing ligand (TRAIL), a member of the TNF superfamily, interacts with its functional death receptors (DRs) and induces apoptosis in a wide range of cancer cell types. Therefore, TRAIL has been considered as an attractive agent for cancer therapy. However, many cancers are resistant to TRAIL-based therapies mainly due to the reduced expression of DRs and/or up-regulation of TRAIL pathway-related anti-apoptotic proteins. Compounds that revert such defects restore the sensitivity of cancer cells to TRAIL, suggesting that combined therapies could help manage neoplastic patients. In this article, we will focus on the TRAIL-sensitizing effects of natural products and synthetic compounds in colorectal cancer (CRC) cells and discuss the molecular mechanisms by which such agents enhance the response of CRC cells to TRAIL. Molecular Diversity Preservation International (MDPI) 2012-06-25 /pmc/articles/PMC3430210/ /pubmed/22942679 http://dx.doi.org/10.3390/ijms13077886 Text en © 2012 by the authors; licensee Molecular Diversity Preservation International, Basel, Switzerland. http://creativecommons.org/licenses/by/3.0 This article is an open-access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).
spellingShingle Review
Stolfi, Carmine
Pallone, Francesco
Monteleone, Giovanni
Molecular Targets of TRAIL-Sensitizing Agents in Colorectal Cancer
title Molecular Targets of TRAIL-Sensitizing Agents in Colorectal Cancer
title_full Molecular Targets of TRAIL-Sensitizing Agents in Colorectal Cancer
title_fullStr Molecular Targets of TRAIL-Sensitizing Agents in Colorectal Cancer
title_full_unstemmed Molecular Targets of TRAIL-Sensitizing Agents in Colorectal Cancer
title_short Molecular Targets of TRAIL-Sensitizing Agents in Colorectal Cancer
title_sort molecular targets of trail-sensitizing agents in colorectal cancer
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3430210/
https://www.ncbi.nlm.nih.gov/pubmed/22942679
http://dx.doi.org/10.3390/ijms13077886
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