ArticleCell death & disease2014
ΔNp63α activates CD82 metastasis suppressor to inhibit cancer cell invasion.
Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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.
The trial behind it
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Who cites it
34 citing papers in PubMed, 50 citations in OpenAlex.
- PRMT5 encourages cell migration and metastasis of tongue squamous cell carcinoma through methylating ΔNp63α.Cell death and differentiation · 2026Article
- TGF-β Signaling in Cancer: Mechanisms of Progression and Therapeutic Targets.International journal of molecular sciences · 2025Review
- ATF6α inhibits ΔNp63α expression to promote breast cancer metastasis by the GRP78-AKT1-FOXO3a signaling.Cell death & disease · 2025Article
- The interaction between ΔNp63α and TAp63α, mediated by miR-205-5p, inhibits the migration of lung adenocarcinoma cells.Scientific reports · 2025Article
- Hypoxia-activated XBP1s recruits HDAC2-EZH2 to engage epigenetic suppression of ΔNp63α expression and promote breast cancer metastasis independent of HIF1α.Cell death and differentiation · 2024Article
- ∆Np63α inhibits Rac1 activation and cancer cell invasion through suppression of PREX1.Cell death discovery · 2024Article
- ΔNp63 Regulates Radioresistance in Human Head and Neck Squamous Carcinoma Cells.Current issues in molecular biology · 2023Article
- Role of a metastatic suppressor gene KAI1/CD82 in the diagnosis and prognosis of breast cancer.Saudi journal of biological sciences · 2021Review
- Toward Colorectal Cancer Biomarkers: The Role of Genetic Variation, Wnt Pathway, and Long Noncoding RNAs.Omics : a journal of integrative biology · 2021Article
- ERK3 is transcriptionally upregulated by ∆Np63α and mediates the role of ∆Np63α in suppressing cell migration in non-melanoma skin cancers.BMC cancer · 2021Article
- Targeting of ΔNp63α by miR-522 promotes the migration of breast epithelial cells.FEBS open bio · 2021Article
- Noncanonical TGF-β signaling leads to FBXO3-mediated degradation of ΔNp63α promoting breast cancer metastasis and poor clinical prognosis.PLoS biology · 2021Article
- From cancer to rejuvenation: incomplete regeneration as the missing link (part II: rejuvenation circle).Future science OA · 2020Review
- Cellular census of human fibrosis defines functionally distinct stromal cell types and states.Nature communications · 2020Article
- Transcriptional suppression of AMPKα1 promotes breast cancer metastasis upon oncogene activation.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- p53-R273H promotes cancer cell migration via upregulation of neuraminidase-1.Journal of Cancer · 2020Article
- ΔNp63 in squamous cell carcinoma: defining the oncogenic routes affecting epigenetic landscape and tumour microenvironment.Molecular oncology · 2019Review
- Serine 195 phosphorylation in the RNA-binding protein Rbm38 increases p63 expression by modulating Rbm38's interaction with the Ago2-miR203 complex.The Journal of biological chemistry · 2019Article
- Role of p53 Family Proteins in Metformin Anti-Cancer Activities.Journal of Cancer · 2019Review
- A double dealing tale of p63: an oncogene or a tumor suppressor.Cellular and molecular life sciences : CMLS · 2018Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
P63 is a p53 family member involved in multiple facets of biology, including embryonic development, cell proliferation, differentiation, survival, apoptosis, senescence and aging. The p63 gene encodes multiple protein isoforms either with (TAp63) or without (ΔNp63) the N-terminal transactivation domain. Amounting evidence suggests that p63 can function as a tumor suppressor, yet the precise molecular mechanisms, and particularly the specific roles of TAp63 and ΔNp63 in cancer progression, are still largely unclear. Here, we demonstrated that ΔNp63α, the predominant isoform expressed in epithelial cells and squamous cell carcinomas, inhibits cell invasion. Affymetrix gene expression profiling, combined with gain- and loss-of-function analyses and chromatin immunoprecipitation, indicated that cluster of differentiation 82 (CD82), a documented metastasis suppressor, is a direct transcriptional target of ΔNp63α. Expression of ΔNp63α inhibited outgrowth in Matrigel and cancer cell invasion, which was largely reversed by specific ablation of CD82. Conversely, ΔNp63α knockdown led to increased cell invasion, which was reversed by ectopic expression of CD82. Moreover, inhibition of glycogen synthase kinase-3β (GSK3β) by either pharmacological inhibitors or by RNA interference resulted in the downregulation of ΔNp63α and CD82 expression, concomitant with increased cell invasion, independently of β-catenin. Furthermore, decreased expression of p63 and CD82 is correlated with cancer progression. Taken together, this study reveals that ΔNp63α upregulates CD82 to inhibit cell invasion, and suggests that GSK3β can regulate cell invasion by modulating the ΔNp63α-CD82 axis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.