Cargando…

Metabolic reprogramming: a bridge between aging and tumorigenesis

Aging is the most robust risk factor for cancer development, with more than 60% of cancers occurring in those aged 60 and above. However, how aging and tumorigenesis are intertwined is poorly understood and a matter of significant debate. Metabolic changes are hallmarks of both aging and tumorigenes...

Descripción completa

Detalles Bibliográficos
Autores principales: Drapela, Stanislav, Ilter, Didem, Gomes, Ana P.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9490145/
https://www.ncbi.nlm.nih.gov/pubmed/35666002
http://dx.doi.org/10.1002/1878-0261.13261
_version_ 1784793027748823040
author Drapela, Stanislav
Ilter, Didem
Gomes, Ana P.
author_facet Drapela, Stanislav
Ilter, Didem
Gomes, Ana P.
author_sort Drapela, Stanislav
collection PubMed
description Aging is the most robust risk factor for cancer development, with more than 60% of cancers occurring in those aged 60 and above. However, how aging and tumorigenesis are intertwined is poorly understood and a matter of significant debate. Metabolic changes are hallmarks of both aging and tumorigenesis. The deleterious consequences of aging include dysfunctional cellular processes, the build‐up of metabolic byproducts and waste molecules in circulation and within tissues, and stiffer connective tissues that impede blood flow and oxygenation. Collectively, these age‐driven changes lead to metabolic reprogramming in different cell types of a given tissue that significantly affects their cellular functions. Here, we put forward the idea that metabolic changes that happen during aging help create a favorable environment for tumorigenesis. We review parallels in metabolic changes that happen during aging and how these changes function both as adaptive mechanisms that enable the development of malignant phenotypes in a cell‐autonomous manner and as mechanisms that suppress immune surveillance, collectively creating the perfect environment for cancers to thrive. Hence, antiaging therapeutic strategies that target the metabolic reprogramming that occurs as we age might provide new opportunities to prevent cancer initiation and/or improve responses to standard‐of‐care anticancer therapies.
format Online
Article
Text
id pubmed-9490145
institution National Center for Biotechnology Information
language English
publishDate 2022
publisher John Wiley and Sons Inc.
record_format MEDLINE/PubMed
spelling pubmed-94901452022-09-30 Metabolic reprogramming: a bridge between aging and tumorigenesis Drapela, Stanislav Ilter, Didem Gomes, Ana P. Mol Oncol Reviews Aging is the most robust risk factor for cancer development, with more than 60% of cancers occurring in those aged 60 and above. However, how aging and tumorigenesis are intertwined is poorly understood and a matter of significant debate. Metabolic changes are hallmarks of both aging and tumorigenesis. The deleterious consequences of aging include dysfunctional cellular processes, the build‐up of metabolic byproducts and waste molecules in circulation and within tissues, and stiffer connective tissues that impede blood flow and oxygenation. Collectively, these age‐driven changes lead to metabolic reprogramming in different cell types of a given tissue that significantly affects their cellular functions. Here, we put forward the idea that metabolic changes that happen during aging help create a favorable environment for tumorigenesis. We review parallels in metabolic changes that happen during aging and how these changes function both as adaptive mechanisms that enable the development of malignant phenotypes in a cell‐autonomous manner and as mechanisms that suppress immune surveillance, collectively creating the perfect environment for cancers to thrive. Hence, antiaging therapeutic strategies that target the metabolic reprogramming that occurs as we age might provide new opportunities to prevent cancer initiation and/or improve responses to standard‐of‐care anticancer therapies. John Wiley and Sons Inc. 2022-06-19 2022-09 /pmc/articles/PMC9490145/ /pubmed/35666002 http://dx.doi.org/10.1002/1878-0261.13261 Text en © 2022 The Authors. Molecular Oncology published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Reviews
Drapela, Stanislav
Ilter, Didem
Gomes, Ana P.
Metabolic reprogramming: a bridge between aging and tumorigenesis
title Metabolic reprogramming: a bridge between aging and tumorigenesis
title_full Metabolic reprogramming: a bridge between aging and tumorigenesis
title_fullStr Metabolic reprogramming: a bridge between aging and tumorigenesis
title_full_unstemmed Metabolic reprogramming: a bridge between aging and tumorigenesis
title_short Metabolic reprogramming: a bridge between aging and tumorigenesis
title_sort metabolic reprogramming: a bridge between aging and tumorigenesis
topic Reviews
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9490145/
https://www.ncbi.nlm.nih.gov/pubmed/35666002
http://dx.doi.org/10.1002/1878-0261.13261
work_keys_str_mv AT drapelastanislav metabolicreprogrammingabridgebetweenagingandtumorigenesis
AT ilterdidem metabolicreprogrammingabridgebetweenagingandtumorigenesis
AT gomesanap metabolicreprogrammingabridgebetweenagingandtumorigenesis