ArticleCell death and differentiation2014
DNA hypermethylation in prostate cancer is a consequence of aberrant epithelial differentiation and hyperproliferation.
Article in Cell death and differentiation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 31 citations in OpenAlex.
- DNA hypermethylation driven by DNMT1 and DNMT3A favors tumor immune escape contributing to the aggressiveness of adrenocortical carcinoma.Clinical epigenetics · 2023Article
- Integrated analysis reveals common DNA methylation patterns of alcohol-associated cancers: A pan-cancer analysis.Frontiers in genetics · 2023Article
- Epigenetic Control of Gene Expression in the Normal and Malignant Human Prostate: A Rapid Response Which Promotes Therapeutic Resistance.International journal of molecular sciences · 2019Review
- Phenotype-independent DNA methylation changes in prostate cancer.British journal of cancer · 2018Article
- MiR-455-3p inhibits the degenerate process of chondrogenic differentiation through modification of DNA methylation.Cell death & disease · 2018Article
- DNA-Methyltransferase 1 Induces Dedifferentiation of Pancreatic Cancer Cells through Silencing of Krüppel-Like Factor 4 Expression.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Article
- Tumor necrosis factor-α decreases EC-SOD expression through DNA methylation.Journal of clinical biochemistry and nutrition · 2017Article
- Exendin-4 promotes extracellular-superoxide dismutase expression in A549 cells through DNA demethylation.Journal of clinical biochemistry and nutrition · 2016Article
- Prostate Cancer Stem-like Cells Contribute to the Development of Castration-Resistant Prostate Cancer.Cancers · 2015Review
- Investigation of methylation and protein expression of theBiomedical reports · 2015Article
- Methylation of PITX2, HOXD3, RASSF1 and TDRD1 predicts biochemical recurrence in high-risk prostate cancer.Journal of cancer research and clinical oncology · 2014Article
- Molecular pathways and targets in prostate cancer.Oncotarget · 2014Review
- DNA methylation profile is associated with the osteogenic potential of three distinct human odontogenic stem cells.Signal transduction and targeted therapyArticle
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostate cancer (CaP) is mostly composed of luminal-like differentiated cells, but contains a small subpopulation of basal cells (including stem-like cells), which can proliferate and differentiate into luminal-like cells. In cancers, CpG island hypermethylation has been associated with gene downregulation, but the causal relationship between the two phenomena is still debated. Here we clarify the origin and function of CpG island hypermethylation in CaP, in the context of a cancer cell hierarchy and epithelial differentiation, by analysis of separated basal and luminal cells from cancers. For a set of genes (including GSTP1) that are hypermethylated in CaP, gene downregulation is the result of cell differentiation and is not cancer specific. Hypermethylation is however seen in more differentiated cancer cells and is promoted by hyperproliferation. These genes are maintained as actively expressed and methylation-free in undifferentiated CaP cells, and their hypermethylation is not essential for either tumour development or expansion. We present evidence for the causes and the dynamics of CpG island hypermethylation in CaP, showing that, for a specific set of genes, promoter methylation is downstream of gene downregulation and is not a driver of gene repression, while gene repression is a result of tissue-specific differentiation.
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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.