Metabolic reprogramming: a bridge between aging and tumorigenesis
Open accessAbstract
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.
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The two hallmarks exhibit commonalities but also differences or antagonisms between aging-associated deregulated nutrient sensing and cancer-associated deregulation of cellular energy metabolism.
“Both hallmarks exhibit clear commonalities, but there are also some differences or even antagonisms between aging-associated deregulated nutrient sensing and cancer-associated deregulation of cellular energy metabolism.[204][205][206]”
From Meta-hallmarks of aging and cancer (2023) · cites this paper as [206]
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- Authors
- Drapela, S., Ilter, D., & Gomes, A. P.
- Affiliations
- Department of Molecular Oncology H. Lee Moffit Cancer Center & Research Institute Tampa FL USA
- Moffitt Cancer Center (US)
- Corresponding author
- Gomes, Ana P.
- Venue
- Molecular Oncology
- Publisher
- Wiley
- Published
- 2022-06-19
- Volume
- 16
- Issue
- 18
- Pages
- 3295-3318
- ISSN
- 1574-7891 (ISSN-L)
- 1878-0261
- PMC
- PMC9490145
- OpenAlex
- W4281620894
- Cited by
- 41
- References
- 256
- Citations by year
- 2026: 11 · 2025: 18 · 2024: 5 · 2023: 4 · 2022: 3
- FWCI
- 0.91
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Molecular Oncology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- American Lung Association
- Florida Breast Cancer Foundation
- National Cancer Institute (R00CA218686)
- NIH Office of the Director (DP2 AG0776980)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- metabolic reprogramming, aging, carcinogenesis, cellular senescence, immune surveillance, cancer prevention, tumor microenvironment, metabolic waste accumulation
- MeSH terms
- Cell Transformation, Neoplastic, Humans, Neoplasms
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