ArticleOncotarget2013
A hidden role of the inactivated FANCD2: upregulating ΔNp63.
Article in Oncotarget, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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.
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Who cites it
14 citing papers in PubMed, 14 citations in OpenAlex.
- Beyond the Double-Strand Breaks: The Role of DNA Repair Proteins in Cancer Stem-Cell Regulation.Cancers · 2021Review
- Gastrointestinal diseases among relatives of patients with esophageal atresia with or without tracheoesophageal fistula.Translational pediatrics · 2019Article
- Multifaceted Fanconi Anemia Signaling.Trends in genetics : TIG · 2018Review
- Fanconi Anemia Signaling and Cancer.Trends in cancer · 2017Review
- Article
- Article
- BLM promotes the activation of Fanconi Anemia signaling pathway.Oncotarget · 2016Article
- FANCI is a negative regulator of Akt activation.Cell cycle (Georgetown, Tex.) · 2016Article
- Mutated Fanconi anemia pathway in non-Fanconi anemia cancers.Oncotarget · 2015Article
- ΔNp63α enhances the oncogenic phenotype of osteosarcoma cells by inducing the expression of GLI2.BMC cancer · 2014Article
- Article
- Basal level of FANCD2 monoubiquitination is required for the maintenance of a sufficient number of licensed-replication origins to fire at a normal rate.Oncotarget · 2014Article
- Advances in the understanding of the Fanconi anemia tumor suppressor pathway.Cancer biology & therapy · 2013Review
- Advances in the understanding of Fanconi Anemia Complementation Group D2 Protein (FANCD2) in human cancer.Cancer cell & microenvironmentArticle
Corrections and comments
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Authors and funding
7 authors at 6 institutions in 2 countries.
Funding
Abstract
A compromised Fanconi Anemia (FA) signaling pathway, often resulting from an inactivated FANCD2, was recently recognized to contribute to the development of non-FA human tumors. However, it is largely unknown as to how an impaired FA pathway or an inactivated FANCD2 promotes tumorigenesis. Here we unexpectedly found that ΔNp63 mRNA was expressed at high levels in human cancer cells carrying an impaired FA pathway compared to the corresponding control cells carrying an intact FA pathway. This observation was recapitulated upon conditionally managing the status of FANCD2 monoubiquitination /activation in 293T cells. Importantly, ΔNp63 elevation upon FANCD2 inactivation was confirmed in human fibroblasts derived from FA patients. Moreover, we have identified a 189 bp DNA fragment downstream of the ΔNp63 promoter (P2) that can mediate the upregulation of ΔNp63 by an inactivated FANCD2, and determined that elevated ΔNp63 is high enough to promote cancer cell proliferation and metastasis. In vivo, the elevation of FAVL, a tumor promotion factor that inhibits FANCD2 activation, was found to be positively associated with ΔNp63 expression in human cancer tissues. Collectively, these results document a novel role of an inactivated FANCD2 in upregulating ΔNp63, advancing our understanding of how an impaired FA pathway contributes to the pathogenesis of human cancer.
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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.