ArticleNeoplasia (New York, N.Y.)2010
Induction of ΔNp63 by the newly identified keratinocyte-specific transforming growth factor β Signaling Pathway with Smad2 and IκB Kinase α in squamous cell carcinoma.
Article in Neoplasia (New York, N.Y.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 15 citations in OpenAlex.
- Complex and variable regulation of ΔNp63 and TAp63 by TGFβ has implications for the dynamics of squamous cell epithelial to mesenchymal transition.Scientific reports · 2024Article
- 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
- Targeted deletion of TGFβ1 in basal keratinocytes causes profound defects in stratified squamous epithelia and aberrant melanocyte migration.Developmental biology · 2022Article
- C-terminal α Domain of p63 Binds to p300 to Coactivate β-Catenin.Neoplasia (New York, N.Y.) · 2019Article
- Transforming growth factor-β1 activates ΔNp63/c-Myc to promote oral squamous cell carcinoma.Oral surgery, oral medicine, oral pathology and oral radiology · 2016Article
- Repression of Wnt/β-catenin response elements by p63 (TP63).Cell cycle (Georgetown, Tex.) · 2016Article
- Overcoming intratumor heterogeneity of polygenic cancer drug resistance with improved biomarker integration.Neoplasia (New York, N.Y.) · 2012Article
- The p63 protein isoform ΔNp63α modulates Y-box binding protein 1 in its subcellular distribution and regulation of cell survival and motility genes.The Journal of biological chemistry · 2012Article
- PAPSS2 promotes alkaline phosphates activity and mineralization of osteoblastic MC3T3-E1 cells by crosstalk and Smads signal pathways.PloS one · 2012Article
- The interconnectedness of cancer cell signaling.Neoplasia (New York, N.Y.) · 2011Article
- Activation of the long terminal repeat of human endogenous retrovirus K by melanoma-specific transcription factor MITF-M.Neoplasia (New York, N.Y.) · 2011Article
- Dinosaurs and ancient civilizations: reflections on the treatment of cancer.Neoplasia (New York, N.Y.) · 2010Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The expression of p63 (TP63/p51) occurs in the basal cells of stratified epithelia and is strongly enhanced at the early stages of squamous cell carcinomas (SCCs) of the head and neck, skin, cervix, and others. We analyzed a promoter/enhancer region (2kΔN) that drives the predominant expression of ΔNp63 for sensitivity to Smad signaling pathways. Reporter assays in HepG2 cells showed a moderate activation of 2kΔN by Smad2 and IκB kinase α (IKKα), partners of the newly identified keratinocyte-specific transforming growth factor β (TGF-β) signaling, but not by other Smad molecules. In A431 cells, 2kΔN was activated by Smad2 and IKKα, for which a Smad binding element (SMD2) at -204 was essential. Binding of Smad2 to the chromosomal SMD2 site was detectable. The association of Smad2 with IKKα was evident in the nucleus of A431, accounting for the enhancement of ΔNp63 expression by TGF-β. Moreover, both ΔNp63 and IKKα were necessary to maintain the noninvasive phenotype of this cell line. FaDu, an invasive, Smad4-deficient SCC, also allowed 2kΔN transactivation by transfected Smad2 in the presence of endogenous IKKα. Reflecting the lack of chromosomal SMD2-Smad2 association and the absence of nuclear IKKα, however, endogenous ΔNp63 was not controlled by TGF-β or IKKα in FaDu. SCC tissue arrays showed nuclear accumulation of IKKα and p63 intensification in well-differentiated noninvasive lesions. This study indicates that p63 is a target gene of the proposed keratinocyte-specific TGF-β signal pathway for suppression of the malignant conversion of SCC.
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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.