Aging and cancer epigenetics: Where do the paths fork?
Open accessAbstract
Aging and cancer are clearly associated processes, at both the epidemiological and molecular level. Epigenetic mechanisms are good candidates to explain the molecular links between the two phenomena, but recent reports have also revealed considerable differences, particularly regarding the loss of DNA methylation in the two processes. The large‐scale generation and availability of genome‐wide epigenetic data now permits systematic studies to be undertaken which may help clarify the similarities and differences between aging and cancer epigenetic alterations. In addition, the development of epigenetic clocks provides a new dimension in which to investigate diseases at the molecular level. Here, we examine current and future questions about the roles of DNA methylation mechanisms as causal factors in the processes of aging and cancer so that we may better understand if and how aging‐associated epigenetic alterations lead to tumorigenesis. It seems certain that comprehending the molecular mechanisms underlying epigenetic clocks, especially with regard to somatic stem cell aging, combined with applying single‐cell epigenetic‐age profiling technologies to aging and cancer cohorts, and the integration of existing and upcoming epigenetic evidence within the genetic damage models of aging will prove to be crucial to improving understanding of these two interrelated phenomena.
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Over the past decade, senescent cells have been shown to promote tumor growth and malignancy through a variety of mechanisms under certain circumstances.
“However, paradoxically, over the past decade, senescent cells have been shown to promote tumor growth and malignancy through a variety of mechanisms under certain circumstances.229–231”
From Drug repurposing for cancer therapy (2024) · cites this paper as [231]
The section on classic aging-associated DNA methylation alterations in cancer says that aging-related changes in the tumor microenvironment may have oncogenic roles, but does not identify senescent cells as the cause. Searches for senescent cells and cellular senescence found no passage in our copy addressing whether such cells promote tumor growth or malignancy through multiple mechanisms. (LLM, conf=0.73)
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“229 – 231 For example, DOX-induced systemic senescence was found to promote metastasis in an orthotopic mouse model of breast cancer.”
Background
- Authors
- Pérez, R. F., Tejedor, J. R., Fernández, A. F., & Fraga, M. F.
- Affiliations
- Consejo Superior de Investigaciones Científicas (ES)
- Corresponding author
- Fernández, Agustín Fernández
- Fraga, Mario Fernández
- Venue
- Aging Cell
- Publisher
- Wiley
- Published
- 2022-09-14
- Volume
- 21
- Issue
- 10
- Pages
- e13709-e13709
- ISSN
- 1474-9718 (ISSN-L)
- 1474-9726
- PMC
- PMC9577950
- OpenAlex
- W4295761495
- Cited by
- 44
- References
- 15
- Citations by year
- 2026: 8 · 2025: 14 · 2024: 8 · 2023: 13 · 2022: 1
- FWCI
- 0.94
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Aging Cell (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion, cc-by)
- Funders
- Fundación Bancaria Caja de Ahorros de Asturias
- Fundación Científica Asociación Española Contra el Cáncer (PROYE18061FERN)
- Fundación General CSIC (0348_CIE_6_E)
- Instituto de Salud Carlos III (PI21/01067)
- Ministerio de Ciencia e Innovación (IJC2018‐36825‐I, SGL2021‐03‐039/40)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- aging, cancer, epigenetics, DNA methylation, epigenetic clocks, carcinogenesis
- MeSH terms
- Aging, Humans, Neoplasms, DNA Methylation, Epigenesis, Genetic, Epigenomics
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