Reversing the aging stromal phenotype prevents carcinoma initiation
Open accessAbstract
The accumulation of senescent stromal cells in aging tissue changes the local microenvironment from normal to a state similar to chronic inflammation. This inflammatory microenvironment can stimulate the proliferation of epithelial cells containing DNA mutations which can ultimately lead to cancer. Using geriatric skin as a model, we demonstrated that senescent fibroblasts also alter how epithelial keratinocytes respond to genotoxic stress, due to the silencing of IGF-1 expression in geriatric fibroblasts. These data indicate that in addition to promoting epithelial tumor growth, senescent fibroblasts also can promote carcinogenic initiation. We hypothesized that commonly used therapeutic stromal wounding therapies can reduce the percentage of senescent fibroblasts and consequently prevent the formation of keratinocytes proliferating with DNA mutations following acute genotoxic (UVB) stress. Sun-protected skin on the lower back of geriatric human volunteers was wounded by dermabrasion and the skin was allowed to heal for three months. In geriatric skin, we found that dermabrasion wounding decreases the proportion of senescent fibroblasts found in geriatric dermis, increases the expression of IGF-1, and restores the appropriate UVB response to epidermal keratinocytes in geriatric skin. Therefore, dermal rejuvenation therapies may play a significant role in preventing the initiation of skin cancer in geriatric patients.
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This is consistent with the reported 20%-60% senescent range of geriatric sun-protected skin fibroblasts.
“consistent with the reported 20%–60% senescent range of geriatric sun-protected skin fibroblasts.40,115”
From Single-cell senescence identification reveals senescence heterogeneity, trajectory, and modulators (2024) · cites this paper as [115]
The Results section, “Senescent fibroblasts accumulate in geriatric dermis in vivo” (page unavailable), reports a significantly increased proportion of senescent fibroblasts in biopsies of sun-protected geriatric skin. It does not report the claimed 20%–60% range in the available text. (LLM, conf=0.87)
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- Authors
- Lewis, D. A., Travers, J. B., Machado, C., Somani, A.-K., & Spandau, D. F.
- Affiliations
- Indiana University Indianapolis (US)
- Corresponding author
- Spandau, Dan F
- Venue
- Aging
- Publisher
- Impact Journals, LLC
- Published
- 2011-04-21
- Volume
- 3
- Issue
- 4
- Pages
- 407-416
- ISSN
- 1945-4589 (ISSN-L)
- PMC
- PMC3117456
- OpenAlex
- W29740597
- Cited by
- 66
- References
- 49
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 3 · 2023: 3 · 2022: 6 · 2021: 10 · 2020: 4 · 2019: 4 · 2018: 4 · 2017: 3 · 2016: 9 · 2015: 3 · 2014: 3 · 2013: 4 · 2012: 3
- FWCI
- 2.62
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by
- Locations
- Aging (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- IUScholarWorks (Indiana University) (submittedVersion, cc-by)
- Funders
- National Institutes of Health
- U.S. Public Health Service (U19A1070448)
- National Heart, Lung, and Blood Institute (R01HL062996)
- National Cancer Institute (R21CA131901)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Dermatology › Skin Protection and Aging
- Health Sciences › Medicine › Rehabilitation › Wound Healing and Treatments
- Keywords
- cellular senescence, senescent fibroblasts, skin aging, carcinogenesis, insulin-like growth factor I, keratinocytes, dermabrasion, chronic inflammation, tumor microenvironment
- MeSH terms
- Aged, Dermabrasion, DNA Damage, Epithelial Cells, Fibroblasts, Humans, Insulin-Like Growth Factor I, Middle Aged, Neoplasms, Phenotype, Skin, Wound Healing, Biomarkers, Keratinocytes, Cellular Senescence, Stromal Cells
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