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Mutant p53 Drives Cancer by Subverting Multiple Tumor Suppression Pathways
The tumor suppressor p53 normally acts as a brake to halt damaged cells from perpetrating their genetic errors into future generations. If p53 is disrupted by mutation, it may not only lose these corrective powers, but counterproductively acquire new capacities that drive cancer. A newly emerging ma...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2016
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4728204/ https://www.ncbi.nlm.nih.gov/pubmed/26858938 http://dx.doi.org/10.3389/fonc.2016.00012 |
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author | Haupt, Sue Raghu, Dinesh Haupt, Ygal |
author_facet | Haupt, Sue Raghu, Dinesh Haupt, Ygal |
author_sort | Haupt, Sue |
collection | PubMed |
description | The tumor suppressor p53 normally acts as a brake to halt damaged cells from perpetrating their genetic errors into future generations. If p53 is disrupted by mutation, it may not only lose these corrective powers, but counterproductively acquire new capacities that drive cancer. A newly emerging manner in which mutant p53 executes its cancer promoting functions is by harnessing key proteins, which normally partner with its wild type, tumor-inhibiting counterpart. In association with the subverted activities of these protein partners, mutant p53 is empowered to act across multiple fundamental cellular pathways (regulating cell division and metabolism) and corrupt them to become cancer promoting. |
format | Online Article Text |
id | pubmed-4728204 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-47282042016-02-08 Mutant p53 Drives Cancer by Subverting Multiple Tumor Suppression Pathways Haupt, Sue Raghu, Dinesh Haupt, Ygal Front Oncol Oncology The tumor suppressor p53 normally acts as a brake to halt damaged cells from perpetrating their genetic errors into future generations. If p53 is disrupted by mutation, it may not only lose these corrective powers, but counterproductively acquire new capacities that drive cancer. A newly emerging manner in which mutant p53 executes its cancer promoting functions is by harnessing key proteins, which normally partner with its wild type, tumor-inhibiting counterpart. In association with the subverted activities of these protein partners, mutant p53 is empowered to act across multiple fundamental cellular pathways (regulating cell division and metabolism) and corrupt them to become cancer promoting. Frontiers Media S.A. 2016-01-27 /pmc/articles/PMC4728204/ /pubmed/26858938 http://dx.doi.org/10.3389/fonc.2016.00012 Text en Copyright © 2016 Haupt, Raghu and Haupt. 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) or licensor 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 | Oncology Haupt, Sue Raghu, Dinesh Haupt, Ygal Mutant p53 Drives Cancer by Subverting Multiple Tumor Suppression Pathways |
title | Mutant p53 Drives Cancer by Subverting Multiple Tumor Suppression Pathways |
title_full | Mutant p53 Drives Cancer by Subverting Multiple Tumor Suppression Pathways |
title_fullStr | Mutant p53 Drives Cancer by Subverting Multiple Tumor Suppression Pathways |
title_full_unstemmed | Mutant p53 Drives Cancer by Subverting Multiple Tumor Suppression Pathways |
title_short | Mutant p53 Drives Cancer by Subverting Multiple Tumor Suppression Pathways |
title_sort | mutant p53 drives cancer by subverting multiple tumor suppression pathways |
topic | Oncology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4728204/ https://www.ncbi.nlm.nih.gov/pubmed/26858938 http://dx.doi.org/10.3389/fonc.2016.00012 |
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