ArticleThe American journal of pathology2011
Expression and regulation of the ΔN and TAp63 isoforms in salivary gland tumorigenesis clinical and experimental findings.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Article
- Development of a New Swine Model Resembling Human Empty Nose Syndrome.Medicina (Kaunas, Lithuania) · 2024Article
- p63 isoforms in triple-negative breast cancer: ΔNp63 associates with the basal phenotype whereas TAp63 associates with androgen receptor, lack of BRCA mutation, PTEN and improved survival.Virchows Archiv : an international journal of pathology · 2018Article
- Article
- An oncogenic MYB feedback loop drives alternate cell fates in adenoid cystic carcinoma.Nature genetics · 2016Article
- The microRNA feedback regulation of p63 in cancer progression.Oncotarget · 2015Review
- Role of the p63-FoxN1 regulatory axis in thymic epithelial cell homeostasis during aging.Cell death & disease · 2013Article
- 15-hydroxyprostaglandin dehydrogenase-derived 15-keto-prostaglandin E2 inhibits cholangiocarcinoma cell growth through interaction with peroxisome proliferator-activated receptor-γ, SMAD2/3, and TAP63 proteins.The Journal of biological chemistry · 2013Article
- Quantitative single cell analysis of cell population dynamics during submandibular salivary gland development and differentiation.Biology open · 2013Article
- Arsenic suppresses cell survival via Pirh2-mediated proteasomal degradation of ΔNp63 protein.The Journal of biological chemistry · 2013Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The TP63 gene, a TP53 homologue, encodes for two main isoforms by different promoters: one retains (TA) and the other lacks (ΔN) the transactivation domain. p63 plays a critical role in the maintenance of basal and myoepithelial cells in ectodermally derived tissues and is implicated in tumorigenesis of several neoplastic entities. However, the biological and regulatory roles of these isoforms in salivary gland tumorigenesis remain unknown. Our results show a reciprocal expression between TA and ΔN isoforms in both benign and malignant salivary tumors. The most dominantly expressed were the ΔN isoforms, whereas the TA isoforms showed generally low levels of expression, except in a few tumors. High ΔNp63 expression characterized tumors with aggressive behavior, whereas tumors with high TAp63 expression were significantly smaller and less aggressive. In salivary gland cells, high expression of ΔNp63 led to enhanced cell migration and invasion and suppression of cell senescence independent of TAp63 and/or TP53 gene status. We conclude the following: i) overexpression of ΔNp63 contributes to salivary tumorigenesis, ii) ΔNp63 plays a dominant negative effect on the TA isoform in the modulation of cell migration and invasion, and iii) the ΔN isoform plays an oncogenic role and may represent an attractive target for therapeutic intervention in patients with salivary carcinomas.
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