Combined CSL and p53 downregulation promotes cancer-associated fibroblast activation
Open accessAbstract
Stromal fibroblast senescence has been linked to ageing-associated cancer risk. However, density and proliferation of cancer-associated fibroblasts (CAFs) are frequently increased. Loss or downmodulation of the Notch effector CSL (also known as RBP-Jκ) in dermal fibroblasts is sufficient for CAF activation and ensuing keratinocyte-derived tumours. We report that CSL silencing induces senescence of primary fibroblasts from dermis, oral mucosa, breast and lung. CSL functions in these cells as a direct repressor of multiple senescence- and CAF-effector genes. It also physically interacts with p53, repressing its activity. CSL is downmodulated in stromal fibroblasts of premalignant skin actinic keratosis lesions and squamous cell carcinomas, whereas p53 expression and function are downmodulated only in the latter, with paracrine FGF signalling as the probable culprit. Concomitant loss of CSL and p53 overcomes fibroblast senescence, enhances expression of CAF effectors and promotes stromal and cancer cell expansion. The findings support a CAF activation-stromal co-evolution model under convergent CSL-p53 control.
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Loss of Notch signalling can promote CAF phenotypes in squamous cell carcinoma, making the Notch mechanism unlikely to be universal.
“however, this mechanism is unlikely to be universal as loss of Notch signalling can promote CAF phenotypes in squamous cell carcinoma56.”
From A framework for advancing our understanding of cancer-associated fibroblasts (2020) · cites this paper as [56]
The Results section (‘CSL as a common repressor of fibroblast senescence and CAF activation’; page unavailable) reports that CSL silencing induces CAF marker genes and that skin SCC-derived CAFs have low CSL levels. But it does not establish that loss of Notch signalling promotes those phenotypes: the same section reports that Notch1 activation also induces CAF-effector genes. The claim conflates loss of the Notch effector CSL with loss of Notch signalling. (LLM, conf=0.86)
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- Authors
- Procopio, M.-G., Laszlo, C., Al Labban, D., Kim, D. E., Bordignon, P., Jo, S.-H., Goruppi, S., Menietti, E., Ostano, P., Ala, U., Provero, P., Hoetzenecker, W., Neel, V., Kilarski, W. W., Swartz, M. A., Brisken, C., Lefort, K., & Dotto, G. P.
- Affiliations
- University of Lausanne (CH)
- Massachusetts General Hospital (US)
- Fondazione Edo ed Elvo Tempia (IT)
- University of Turin (IT)
- University of Zurich (CH)
- École Polytechnique Fédérale de Lausanne (CH)
- Centre Hospitalier Universitaire Vaudois (CH)
- Corresponding author
- Dotto, G. Paolo
- ORCID
- Venue
- Nature Cell Biology
- Published
- 2015-08-24
- Volume
- 17
- Issue
- 9
- Pages
- 1193-1204
- ISSN
- 1465-7392 (ISSN-L)
- 1476-4679
- PMC
- PMC4699446
- OpenAlex
- W2123584388
- Cited by
- 223
- References
- 69
- Citations by year
- 2026: 9 · 2025: 10 · 2024: 19 · 2023: 18 · 2022: 20 · 2021: 28 · 2020: 31 · 2019: 25 · 2018: 24 · 2017: 17 · 2016: 20 · 2015: 1 · 2014: 1
- FWCI
- 15.22
- Type
- journal article
- Language
- en
- Update notices
- erratum (2015-09-30)
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- SERVAL (Université de Lausanne) (publishedVersion)
- PubMed Central (acceptedVersion)
- IRIS (submittedVersion)
- Institutional Research Information System University of Turin (University of Turin) (submittedVersion, other-oa)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion, cc-by-nc-nd)
- Funders
- National Science Foundation
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (156191, 310030_156191/1, 310030)
- Oncosuisse (OCS-2922-02-2012)
- National Institutes of Health
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR039190, R01AR064786)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- CSL, RBP-Jκ, p53, cancer-associated fibroblasts, fibroblast senescence, Notch signaling, stromal fibroblasts, actinic keratosis, squamous cell carcinoma, FGF signaling, tumor microenvironment, tumor stroma
- MeSH terms
- Animals, Carcinoma, Squamous Cell, Fibroblasts, Humans, Skin Neoplasms, Signal Transduction, Down-Regulation, Gene Expression Regulation, Neoplastic, Tumor Suppressor Protein p53, Cellular Senescence, Receptors, Fibroblast Growth Factor, Cell Line, Tumor, Mice, Immunoglobulin J Recombination Signal Sequence-Binding Protein
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