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ΔNp63α Is an Oncogene that Targets Chromatin Remodeler Lsh to Drive Skin Stem Cell Proliferation and Tumorigenesis
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SUMMARY The p53 homolog p63 is essential for development, yet its role in cancer is not clear. We discovered that p63 deficiency evokes the tumor suppressive mechanism of cellular senescence, causing a striking absence of stratified epithelia such as the skin. Here we identify the predominant p63 isoform, ΔNp63α, as a protein that bypasses oncogene induced senescence to drive tumorigenesis in vivo. Interestingly, bypass of senescence promotes stem-like proliferation and maintains survival of the keratin 15-positive stem cell population. Furthermore, we identify the chromatin remodeling protein Lsh as a new target of ΔNp63α that is an essential mediator of senescence bypass. These findings indicate that ΔNp63α is an oncogene that cooperates with Ras to promote tumor-initiating stem-like proliferation, and suggest that Lsh-mediated chromatin remodeling events are critical to this process.
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“Specific TFs were also essential, including TP63, the epidermal master regulator and cSCC oncogene (Keyes et al., 2011), as well as the AP1 family TFs, FOSL1 and JUNB.”
From Multimodal Analysis of Composition and Spatial Architecture in Human Squamous Cell Carcinoma (2020) · cites this paper as Keyes et al., 2011
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p63 is essential for regenerative proliferation in limb, craniofacial and epithelial development
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“RESULTS SETDB1 is required for SCC cell survival and maintenance of stem-like cancer cells We previously connected chromatin remodeling proteins to SCC progression and maintenance of stem-like cancer cells [14, 30].”
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“This is in agreement with findings indicating that overexpression of the ΔNp63a isoform blocks replicative senescence mediated by p16 and p19 inhibition and cooperates with Ras to maintain the stem cell population of mouse keratinocytes, promoting their malignant conversion (Ha et al., 2011; Keyes et al., 2011).”
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“promoting their malignant conversion by EpithelialMesenchymal Transition (EMT) process.(47) In addition,”
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“Interestingly authors found that the common motifs between IFE and Epcam+ TECs, significantly upregulated during tumorigenesis are Jun/AP1 (58%), p63 (43%), and Klf (22%), suggesting that p63 and Klf5 transcriptional factors contribute to the epigenetic priming to give rise to well-differentiated tumors without EMT in…”
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“HELLS is mutated or misregulated in tumour samples from several cancer types (Yano et al., 2004; Kim et al., 2010; Janus et al., 2011; Keyes et al., 2011; Von Eyss et al., 2012) and is also mutated in some cases of immunodeficiency-centromeric instability-facial anomalies syndrome (ICF), which is…”
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Metadata
- Authors
- Keyes, W. M., Pecoraro, M., Aranda, V., Vernersson-Lindahl, E., Li, W., Vogel, H., Guo, X., Garcia, E. L., Michurina, T. V., Enikolopov, G., Muthuswamy, S. K., & Mills, A. A.
- Affiliations
- Cold Spring Harbor Laboratory (US)
- Universitat Pompeu Fabra (ES)
- Stanford Medicine (US)
- University of Toronto (CA)
- Corresponding author
- Keyes, William M.
- Mills, Alea A.
- ORCID
- Venue
- Cell Stem Cell
- Publisher
- Elsevier BV
- Published
- 2011-02
- Volume
- 8
- Issue
- 2
- Pages
- 164-176
- ISSN
- 1875-9777 (ISSN-L)
- 1934-5909
- PMC
- PMC4373450
- OpenAlex
- W2005062632
- Semantic Scholar
- c1f79d43c5cb2d63b4b44bf6992e804b60c11dd7
- Cited by
- 193
- References
- 53
- Citations by year
- 2026: 6 · 2025: 3 · 2024: 11 · 2023: 8 · 2022: 5 · 2021: 14 · 2020: 12 · 2019: 14 · 2018: 13 · 2017: 17 · 2016: 18 · 2015: 6 · 2014: 18 · 2013: 18 · 2012: 17
- FWCI
- 14.39
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell stem cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Cold Spring Harbor Laboratory Institutional Repository (Cold Spring Harbor Laboratory) (acceptedVersion)
- Repositori digital de la UPF (Universitat Pompeu Fabra) (submittedVersion, other-oa)
- Funders
- National Cancer Institute (R01CA098830)
- 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 › Molecular Biology › Chromatin Remodeling and Cancer
- Keywords
- ΔNp63α, p63 isoforms, LSH, chromatin remodeling, oncogenes, senescence bypass, oncogene-induced senescence, skin stem cells, keratin 15, stem cell proliferation, carcinogenesis, stratified epithelium, skin cancer
- MeSH terms
- Animals, Cells, Cultured, DNA Helicases, Flow Cytometry, Humans, Mice, Nude, Phosphoproteins, Protein Binding, Skin, Stem Cells, Trans-Activators, Keratinocytes, Polymerase Chain Reaction, Chromatin Immunoprecipitation, Cell Proliferation, Mice
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