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Ataxia-Telangiectasia Mutated Modulation of Carbon Metabolism in Cancer
The ataxia-telangiectasia mutated (ATM) protein kinase has been extensively studied for its role in the DNA damage response and its association with the disease ataxia telangiectasia. There is increasing evidence that ATM also plays an important role in other cellular processes, including carbon met...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5712564/ https://www.ncbi.nlm.nih.gov/pubmed/29238697 http://dx.doi.org/10.3389/fonc.2017.00291 |
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author | Dahl, Erika S. Aird, Katherine M. |
author_facet | Dahl, Erika S. Aird, Katherine M. |
author_sort | Dahl, Erika S. |
collection | PubMed |
description | The ataxia-telangiectasia mutated (ATM) protein kinase has been extensively studied for its role in the DNA damage response and its association with the disease ataxia telangiectasia. There is increasing evidence that ATM also plays an important role in other cellular processes, including carbon metabolism. Carbon metabolism is highly dysregulated in cancer due to the increased need for cellular biomass. A number of recent studies report a non-canonical role for ATM in the regulation of carbon metabolism. This review highlights what is currently known about ATM’s regulation of carbon metabolism, the implication of these pathways in cancer, and the development of ATM inhibitors as therapeutic strategies for cancer. |
format | Online Article Text |
id | pubmed-5712564 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-57125642017-12-13 Ataxia-Telangiectasia Mutated Modulation of Carbon Metabolism in Cancer Dahl, Erika S. Aird, Katherine M. Front Oncol Oncology The ataxia-telangiectasia mutated (ATM) protein kinase has been extensively studied for its role in the DNA damage response and its association with the disease ataxia telangiectasia. There is increasing evidence that ATM also plays an important role in other cellular processes, including carbon metabolism. Carbon metabolism is highly dysregulated in cancer due to the increased need for cellular biomass. A number of recent studies report a non-canonical role for ATM in the regulation of carbon metabolism. This review highlights what is currently known about ATM’s regulation of carbon metabolism, the implication of these pathways in cancer, and the development of ATM inhibitors as therapeutic strategies for cancer. Frontiers Media S.A. 2017-11-29 /pmc/articles/PMC5712564/ /pubmed/29238697 http://dx.doi.org/10.3389/fonc.2017.00291 Text en Copyright © 2017 Dahl and Aird. 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 Dahl, Erika S. Aird, Katherine M. Ataxia-Telangiectasia Mutated Modulation of Carbon Metabolism in Cancer |
title | Ataxia-Telangiectasia Mutated Modulation of Carbon Metabolism in Cancer |
title_full | Ataxia-Telangiectasia Mutated Modulation of Carbon Metabolism in Cancer |
title_fullStr | Ataxia-Telangiectasia Mutated Modulation of Carbon Metabolism in Cancer |
title_full_unstemmed | Ataxia-Telangiectasia Mutated Modulation of Carbon Metabolism in Cancer |
title_short | Ataxia-Telangiectasia Mutated Modulation of Carbon Metabolism in Cancer |
title_sort | ataxia-telangiectasia mutated modulation of carbon metabolism in cancer |
topic | Oncology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5712564/ https://www.ncbi.nlm.nih.gov/pubmed/29238697 http://dx.doi.org/10.3389/fonc.2017.00291 |
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