ArticleOncogene2003
Mutant p53 and aberrant cytosine methylation cooperate to silence gene expression.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 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.
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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
50 citing papers in PubMed, 98 citations in OpenAlex.
- Association of DSC3 mRNA down-regulation in prostate cancer with promoter hypermethylation and poor prognosis.PloS one · 2014Trial
- Increased reflux secondary bile acids are associated with changes to the microbiome and transcriptome in Barrett's esophagus.Gut microbes · 2025Article
- Desmocollin-3 and Bladder Cancer.Diseases (Basel, Switzerland) · 2025Article
- Expression and associated epigenetic mechanisms of the CaJournal of cell communication and signaling · 2022Article
- Estradiol-mediated inhibition of DNMT1 decreases p53 expression to induce M2-macrophage polarization in lung cancer progression.Oncogenesis · 2022Article
- Integrating the tumor-suppressive activity of Maspin with p53 in retuning the epithelial homeostasis: A working hypothesis and applicable prospects.Frontiers in oncology · 2022Review
- Role of class I histone deacetylases in the regulation of maspin expression in prostate cancer.Molecular carcinogenesis · 2020Article
- Maspin subcellular expression in wild-type and mutantWorld journal of gastrointestinal oncology · 2020Article
- Wild-type p53 regulates OTOP2 transcription through DNA loop alteration of the promoter in colorectal cancer.FEBS open bio · 2019Article
- Upregulation of maspin expression in human cervical carcinoma cells by transforming growth factor β1 through the convergence of Smad and non-Smad signaling pathways.Oncology letters · 2017Article
- Article
- The isolation of an RNA aptamer targeting to p53 protein with single amino acid mutation.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- A lincRNA connected to cell mortality and epigenetically-silenced in most common human cancers.Epigenetics · 2015Article
- Desmosomes: regulators of cellular signaling and adhesion in epidermal health and disease.Cold Spring Harbor perspectives in medicine · 2014Review
- Expression and localization of maspin in cervical cancer and its role in tumor progression and lymphangiogenesis.Archives of gynecology and obstetrics · 2014Article
- Plakoglobin as a regulator of desmocollin gene expression.The Journal of investigative dermatology · 2013Article
- Characterization of synergistic anti-cancer effects of docosahexaenoic acid and curcumin on DMBA-induced mammary tumorigenesis in mice.BMC cancer · 2013Article
- Epigenetic therapies as a promising strategy for overcoming chemoresistance in epithelial ovarian cancer.Journal of cancer prevention · 2013Review
- Role of maspin in cancer.Clinical and translational medicine · 2013Article
- miRNA gene promoters are frequent targets of aberrant DNA methylation in human breast cancer.PloS one · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
p53 is an important transcriptional regulator that is frequently mutated in cancer. Gene-profiling experiments of breast cancer cells infected with wt p53 revealed both MASPIN and desmocollin 3 (DSC3) to be p53-target genes, even though both genes are silenced in association with aberrant cytosine methylation of their promoters. Despite the transcriptional repression of these genes by aberrant DNA methylation, restoration of p53 resulted in the partial reactivation of both genes. This reactivation is a result of wt p53 binding to its consensus DNA-binding sites within the MASPIN and DSC3 promoters, stimulating histone acetylation, and enhancing chromatin accessibility of their promoters. Interestingly, wt p53 alone did not affect the methylation status of either promoter, suggesting that p53 itself can partially overcome the repressive barrier of DNA methylation. Pharmacologic inhibition of DNA methylation with 5-aza-2'-deoxycytidine in combination with restoration of wt p53 status resulted in a synergistic reactivation of these genes to near-normal levels. These results suggest that cancer treatments that target both genetic and epigenetic facets of gene regulation may be a useful strategy towards the therapeutic transcriptional reprogramming of cancer cells.
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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.