ArticlePloS one2011
Dysregulated ΔNp63α inhibits expression of Ink4a/arf, blocks senescence, and promotes malignant conversion of keratinocytes.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
22 citing papers in PubMed, 42 citations in OpenAlex.
- p63 and ZNF148 cooperate to regulate head and neck squamous cell carcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Long-Term Expansion of Mouse Primary Epidermal Keratinocytes Using a TGF-β Signaling Inhibitor.Methods in molecular biology (Clifton, N.J.) · 2025Article
- SE-lncRNAs in Cancer: Classification, Subcellular Localisation, Function and Corresponding TFs.Journal of cellular and molecular medicine · 2024Review
- Oncogenic Ras and ΔNp63α cooperate to recruit immunosuppressive polymorphonuclear myeloid-derived suppressor cells in a mouse model of squamous cancer pathogenesis.Frontiers in immunology · 2023Article
- RAS oncogene signal strength regulates matrisomal gene expression and tumorigenicity of mouse keratinocytes.Carcinogenesis · 2022Article
- DNA Demethylation Switches Oncogenic ΔNp63 to Tumor Suppressive TAp63 in Squamous Cell Carcinoma.Frontiers in oncology · 2022Article
- RAS induced senescence of skin keratinocytes is mediated through Rho-associated protein kinase (ROCK).Molecular carcinogenesis · 2021Article
- Oh, the Mutations You'll Acquire! A Systematic Overview of Cutaneous Squamous Cell Carcinoma.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2021Review
- Cutaneous Squamous Cell Carcinoma: From Pathophysiology to Novel Therapeutic Approaches.Biomedicines · 2021Review
- Loss of oral mucosal stem cell markers in oral submucous fibrosis and their reactivation in malignant transformation.International journal of oral science · 2020Review
- Knockdown of Long Non-Coding RNA (lncRNA) Colon Cancer-Associated Transcript-1 (CCAT1) Suppresses Oral Squamous Cell Carcinoma Proliferation, Invasion, and Migration by Inhibiting the Discoidin Domain Receptor 2 (DDR2)/ERK/AKT Axis.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- p63 Is a Promising Marker in the Diagnosis of Unusual Skin Cancer.International journal of molecular sciences · 2019Review
- Molecular Mechanisms of p63-Mediated Squamous Cancer Pathogenesis.International journal of molecular sciences · 2019Review
- Co-activation of super-enhancer-driven CCAT1 by TP63 and SOX2 promotes squamous cancer progression.Nature communications · 2018Article
- PKK deletion in basal keratinocytes promotes tumorigenesis after chemical carcinogenesis.Carcinogenesis · 2018Article
- Inhibition of TGF-β signaling supports high proliferative potential of diverse p63Scientific reports · 2017Article
- ACTL6A Is Co-Amplified with p63 in Squamous Cell Carcinoma to Drive YAP Activation, Regenerative Proliferation, and Poor Prognosis.Cancer cell · 2017Article
- The homeoprotein DLX3 and tumor suppressor p53 co-regulate cell cycle progression and squamous tumor growth.Oncogene · 2016Article
- ΔNp63 regulates IL-33 and IL-31 signaling in atopic dermatitis.Cell death and differentiation · 2016Article
- Delineating Molecular Mechanisms of Squamous Tissue Homeostasis and Neoplasia: Focus on p63.Journal of skin cancer · 2013Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
p63 is critical for squamous epithelial development, and elevated levels of the ΔNp63α isoform are seen in squamous cell cancers of various organ sites. However, significant controversy exists regarding the role of p63 isoforms as oncoproteins or tumor suppressors. Here, lentiviruses were developed to drive long-term overexpression of ΔNp63α in primary keratinocytes. Elevated levels of ΔNp63α in vitro promote long-term survival and block both replicative and oncogene-induced senescence in primary keratinocytes, as evidenced by the expression of SA-β-gal and the presence of nuclear foci of heterochromatin protein 1γ. The contribution of ΔNp63α to cancer development was assessed using an in vivo grafting model of experimental skin tumorigenesis that allows distinction between benign and malignant tumors. Grafted lenti-ΔNp63α keratinocytes do not form tumors, whereas lenti-GFP/v-ras(Ha) keratinocytes develop well-differentiated papillomas. Lenti-ΔNp63α/v-ras(Ha) keratinocytes form undifferentiated carcinomas. The average volume of lenti-ΔNp63α/v-ras(Ha) tumors was significantly higher than those in the lenti-GFP/v-ras(Ha) group, consistent with increased BrdU incorporation detected by immunohistochemistry. The block in oncogene-induced senescence corresponds to sustained levels of E2F1 and phosphorylated AKT, and is associated with loss of induction of p16(ink4a)/p19(arf). The relevance of p16(ink4a)/p19(arf) loss was demonstrated in grafting studies of p19(arf)-null keratinocytes, which develop malignant carcinomas in the presence of v-ras(Ha) similar to those arising in wildtype keratinocytes that express lenti-ΔNp63α and v-ras(Ha). Our findings establish that ΔNp63α has oncogenic activity and its overexpression in human squamous cell carcinomas contributes to the malignant phenotype, and implicate its ability to regulate p16(ink4a)/p19(arf) in the process.
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