ArticleBMC cancer2008
A limited role for p53 in modulating the immediate phenotype of Apc loss in the intestine.
Article in BMC cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- Colorectal cancer murine models: Initiation to metastasis.Cancer letters · 2024Review
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- 29 mJournal of immunology research · 2022Article
- Organelle Crosstalk Regulators Are Regulated in Diseases, Tumors, and Regulatory T Cells: Novel Classification of Organelle Crosstalk Regulators.Frontiers in cardiovascular medicine · 2021Article
- Compensation between Wnt-driven tumorigenesis and cellular responses to ribosome biogenesis inhibition in the murine intestinal epithelium.Cell death and differentiation · 2020Article
- ANIMAL MODELS FOR COLORECTAL CANCER.Arquivos brasileiros de cirurgia digestiva : ABCD = Brazilian archives of digestive surgery · 2018Review
- PTEN loss and activation of K-RAS and β-catenin cooperate to accelerate prostate tumourigenesis.The Journal of pathology · 2017Article
- Cellular context-dependent consequences of Apc mutations on gene regulation and cellular behavior.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Article
- Opposing effects of TIGAR- and RAC1-derived ROS on Wnt-driven proliferation in the mouse intestine.Genes & development · 2016Article
- Article
- Inducible in vivo genome editing with CRISPR-Cas9.Nature biotechnology · 2015Article
- Comprehensive analysis of β-catenin target genes in colorectal carcinoma cell lines with deregulated Wnt/β-catenin signaling.BMC genomics · 2014Article
- Animal models of colorectal cancer.Cancer metastasis reviews · 2013Review
- Article
- CD44 expression in intestinal epithelium and colorectal cancer is independent of p53 status.PloS one · 2013Article
- Liver cancer initiation is controlled by AP-1 through SIRT6-dependent inhibition of survivin.Nature cell biology · 2012Article
- Article
- Corruption of homeostatic mechanisms in the guanylyl cyclase C signaling pathway underlying colorectal tumorigenesis.Cancer biology & therapy · 2010Review
- Acute overexpression of Myc in intestinal epithelium recapitulates some but not all the changes elicited by Wnt/beta-catenin pathway activation.Molecular and cellular biology · 2009Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundp53 is an important tumour suppressor with a known role in the later stages of colorectal cancer, but its relevance to the early stages of neoplastic initiation remains somewhat unclear. Although p53-dependent regulation of Wnt signalling activity is known to occur, the importance of these regulatory mechanisms during the early stages of intestinal neoplasia has not been demonstrated.
methodsWe have conditionally deleted the Adenomatous Polyposis coli gene (Apc) from the adult murine intestine in wild type and p53 deficient environments and subsequently compared the phenotype and transcriptome profiles in both genotypes.
resultsExpression of p53 was shown to be elevated following the conditional deletion of Apc in the adult small intestine. Furthermore, p53 status was shown to impact on the transcription profile observed following Apc loss. A number of key Wnt pathway components and targets were altered in the p53 deficient environment. However, the aberrant phenotype observed following loss of Apc (rapid nuclear localisation of beta-catenin, increased levels of DNA damage, nuclear atypia, perturbed cell death, proliferation, differentiation and migration) was not significantly altered by the absence of p53.
conclusionp53 related feedback mechanisms regulating Wnt signalling activity are present in the intestine, and become activated following loss of Apc. However, the physiological Wnt pathway regulation by p53 appears to be overwhelmed by Apc loss and consequently the activity of these regulatory mechanisms is not sufficient to modulate the immediate phenotypes seen following Apc loss. Thus we are able to provide an explanation to the apparent contradiction that, despite having a Wnt regulatory capacity, p53 loss is not associated with early lesion development.
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