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The p53/Adipose-Tissue/Cancer Nexus
Obesity and the resultant metabolic complications have been associated with an increased risk of cancer. In addition to the systemic metabolic disturbances in obesity that are associated with cancer initiation and progression, the presence of adipose tissue in the tumor microenvironment (TME) contri...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2018
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6104444/ https://www.ncbi.nlm.nih.gov/pubmed/30158901 http://dx.doi.org/10.3389/fendo.2018.00457 |
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author | Zwezdaryk, Kevin Sullivan, Deborah Saifudeen, Zubaida |
author_facet | Zwezdaryk, Kevin Sullivan, Deborah Saifudeen, Zubaida |
author_sort | Zwezdaryk, Kevin |
collection | PubMed |
description | Obesity and the resultant metabolic complications have been associated with an increased risk of cancer. In addition to the systemic metabolic disturbances in obesity that are associated with cancer initiation and progression, the presence of adipose tissue in the tumor microenvironment (TME) contributes significantly to malignancy through direct cell-cell interaction or paracrine signaling. This chronic inflammatory state can be maintained by p53-associated mechanisms. Increased p53 levels that are observed in obesity exacerbate the release of inflammatory cytokines that fuel cancer initiation and progression. Dysregulated adipose tissue signaling from the TME can reprogram tumor cell metabolism. The links between p53, cellular metabolism and adipose tissue dysfunction and how they relate to cancer, will be presented in this review. |
format | Online Article Text |
id | pubmed-6104444 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-61044442018-08-29 The p53/Adipose-Tissue/Cancer Nexus Zwezdaryk, Kevin Sullivan, Deborah Saifudeen, Zubaida Front Endocrinol (Lausanne) Endocrinology Obesity and the resultant metabolic complications have been associated with an increased risk of cancer. In addition to the systemic metabolic disturbances in obesity that are associated with cancer initiation and progression, the presence of adipose tissue in the tumor microenvironment (TME) contributes significantly to malignancy through direct cell-cell interaction or paracrine signaling. This chronic inflammatory state can be maintained by p53-associated mechanisms. Increased p53 levels that are observed in obesity exacerbate the release of inflammatory cytokines that fuel cancer initiation and progression. Dysregulated adipose tissue signaling from the TME can reprogram tumor cell metabolism. The links between p53, cellular metabolism and adipose tissue dysfunction and how they relate to cancer, will be presented in this review. Frontiers Media S.A. 2018-08-14 /pmc/articles/PMC6104444/ /pubmed/30158901 http://dx.doi.org/10.3389/fendo.2018.00457 Text en Copyright © 2018 Zwezdaryk, Sullivan and Saifudeen. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Endocrinology Zwezdaryk, Kevin Sullivan, Deborah Saifudeen, Zubaida The p53/Adipose-Tissue/Cancer Nexus |
title | The p53/Adipose-Tissue/Cancer Nexus |
title_full | The p53/Adipose-Tissue/Cancer Nexus |
title_fullStr | The p53/Adipose-Tissue/Cancer Nexus |
title_full_unstemmed | The p53/Adipose-Tissue/Cancer Nexus |
title_short | The p53/Adipose-Tissue/Cancer Nexus |
title_sort | p53/adipose-tissue/cancer nexus |
topic | Endocrinology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6104444/ https://www.ncbi.nlm.nih.gov/pubmed/30158901 http://dx.doi.org/10.3389/fendo.2018.00457 |
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