ArticleOncogene2008
p73 expression modulates p63 and Mdm2 protein presence in complex with p53 family-specific DNA target sequence in squamous cell carcinogenesis.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- The interplay between Epstein-Bar virus (EBV) with the p53 and its homologs during EBV associated malignancies.Heliyon · 2019Review
- Emodin promotes the arrest of human lymphoma Raji cell proliferation through the UHRF1‑DNMT3A‑∆Np73 pathways.Molecular medicine reports · 2017Article
- p53 Family: Role of Protein Isoforms in Human Cancer.Journal of nucleic acids · 2012Article
- Manganese superoxide dismutase is a p53-regulated gene that switches cancers between early and advanced stages.Cancer research · 2011Article
- Recent advances in validating MDM2 as a cancer target.Anti-cancer agents in medicinal chemistry · 2009Review
- Therapeutic prospects for p73 and p63: rising from the shadow of p53.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The expression of p73 and p63 isoforms is frequently deregulated in human epithelial tumors. We previously showed that loss of p73 protein expression associates with malignant conversion in vivo and ionizing radiation (IR) resistance in vitro in a clonal model of mouse epidermal carcinogenesis. Here we show that loss of endogenous p73 expression in squamous cell carcinoma (SCC) cells and tumors was concomitant with preferential DNA binding of the inhibitory DeltaNp63alpha isoform and reduction of transcriptionally active p63gamma isoforms binding to a p21 promoter sequence in vitro. Reconstitution of TAp73alpha in malignant cells increased the steady state DNA-binding capabilities of the endogenous transcriptionally active TAp63gamma and DeltaNp63gamma isoforms, correlating with restoration of tumor suppression but not IR sensitivity. Loss of p73 in malignant cells also coincided with increased presence of p53 family inhibitor Mdm2 in p53-specific DNA-bound complexes, whereas reconstitution of TAp73alpha expression resulted in exclusion of Mdm2 from these complexes. These results suggest a dual mechanism for TAp73alpha to foster tumor suppression through enhancement of the DNA-binding activity of p63gamma isoforms, and through inhibition of transcriptional repressors Mdm2 or DeltaNp63alpha.
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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.