The DOI matches its Crossref record; 42 of the 43 references it cites were found in a registry or an index.
WNT16B Is a New Marker of Cellular Senescence That Regulates p53 Activity and the Phosphoinositide 3-Kinase/AKT Pathway
Open accessPublished version of a preprint
Abstract
Senescence is a tumor suppression mechanism that is induced by several stimuli, including oncogenic signaling and telomere shortening, and controlled by the p53/p21WAF1 signaling pathway. Recently, a critical role for secreted factors has emerged, suggesting that extracellular signals are necessary for the onset and maintenance of senescence. Conversely, factors secreted by senescent cells may promote tumor growth. By using expression profiling techniques, we searched for secreted factors that were overexpressed in fibroblasts undergoing replicative senescence. We identified WNT16B, a member of the WNT family of secreted proteins. We found that WNT16B is overexpressed in cells undergoing stress-induced premature senescence and oncogene-induced senescence in both MRC5 cell line and the in vivo murine model of K-RasV12–induced senescence. By small interfering RNA experiments, we observed that both p53 and WNT16B are necessary for the onset of replicative senescence. WNT16B expression is required for the full transcriptional activation of p21WAF1. Moreover, WNT16B regulates activation of the phosphoinositide 3-kinase (PI3K)/AKT pathway. Overall, we identified WNT16B as a new marker of senescence that regulates p53 activity and the PI3K/AKT pathway and is necessary for the onset of replicative senescence. [Cancer Res 2009;69(24):9183–91]
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“Likewise, secreted WNT16B is an important enforcer of the senescence growth arrest of human fibroblasts in culture, as well as that of mouse cells that senesce in vivo owing to expression of an activated RAS oncogene (138).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [138]
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BackgroundInfluentialSelf-citationExtension of Life-Span by Introduction of Telomerase into Normal Human Cells
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Chemokine signaling via the CXCR2 receptor reinforces senescence
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“org Downloaded from cence (SIPS), can be induced by events such as DNA damage (4), oxidative stress (5), epigenetic modifications (6), or cytokine stimulation (7).”
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Stoffel, M., Baschun, K., Kehl, M., Ellinger, J., Klümper, N., Kadzik, S., Winterhagen, F. I., Ritter, M., Hölzel, M., Kristiansen, G., et al. (2026) · BMC Cancer · doi:10.1186/s12885-026-17178-6
Jiang, Y., Zhang, Q., Yang, H., Zhou, Y., Zhao, L., Yao, Y., & Peng, J. (2026) · Coordination Chemistry Reviews · doi:10.1016/j.ccr.2026.218702
Metadata
- Authors
- Binet, R., Ythier, D., Robles, A. I., Collado, M., Larrieu, D., Fonti, C., Brambilla, E., Brambilla, C., Serrano, M., Harris, C. C., & Pedeux, R.
- Affiliations
- Inserm (FR)
- Corresponding author
- Pedeux, Rémy
- ORCID
- Venue
- Cancer Research
- Published
- 2009-12-14
- Volume
- 69
- Issue
- 24
- Pages
- 9183-9191
- ISSN
- 0008-5472 (ISSN-L)
- 1538-7445
- PMC
- PMC7439003
- OpenAlex
- W2123104757
- Cited by
- 101
- References
- 43
- Citations by year
- 2026: 1 · 2025: 5 · 2024: 5 · 2023: 3 · 2022: 3 · 2021: 4 · 2020: 7 · 2019: 6 · 2018: 3 · 2017: 5 · 2016: 9 · 2015: 9 · 2014: 10 · 2013: 8 · 2012: 6
- FWCI
- 5.10
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute (Z01BC005794)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- cellular senescence, replicative senescence, stress-induced premature senescence, oncogene-induced senescence, p53, p21, PI3K/Akt signaling, secreted factors, fibroblasts, tumor suppression, senescence-associated secretory phenotype
- MeSH terms
- Phosphoinositide-3 Kinase Inhibitors, Chromones, Enzyme Inhibitors, Fibroblasts, Humans, Morpholines, Transcription, Genetic, Transfection, Tumor Suppressor Protein p53, Cellular Senescence, Phosphatidylinositol 3-Kinases, Oligonucleotide Array Sequence Analysis, Gene Expression Profiling, RNA, Small Interfering, Cyclin-Dependent Kinase Inhibitor p21, Proto-Oncogene Proteins c-akt, Wnt Proteins
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