ArticleCell & bioscience2018
Epigenetic alterations in TRAMP mice: epigenome DNA methylation profiling using MeDIP-seq.
Article in Cell & bioscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Tributyltin chloride alters the structural, genomic, and epigenomic integrity of postejaculatory mammalian sperm.Epigenetics · 2025Article
- Epigenetic reprogramming during prostate cancer progression: A perspective from development.Seminars in cancer biology · 2022Review
- Epigenetics/Epigenomics and Prevention of Early Stages of Cancer by Isothiocyanates.Cancer prevention research (Philadelphia, Pa.) · 2021Review
- Screening and Identification of Key Biomarkers for Bladder Cancer: A Study Based on TCGA and GEO Data.BioMed research international · 2020Article
- Differentially Expressed Genes and Molecular Pathways in an Autochthonous Mouse Prostate Cancer Model.Frontiers in genetics · 2019Article
- Exploration of bladder cancer-associated methylated miRNAs by methylated DNA immunoprecipitation sequencing.OncoTargets and therapy · 2019Article
- Cancer-associated methylated lncRNAs in patients with bladder cancer.American journal of translational research · 2019Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
purposeWe investigated the genomic DNA methylation profile of prostate cancer in transgenic adenocarcinoma of the mouse prostate (TRAMP) cancer model and to analyze the crosstalk among targeted genes and the related functional pathways.
methodsProstate DNA samples from 24-week-old TRAMP and C57BL/6 male mice were isolated. The DNA methylation profiles were analyzed by methylated DNA immunoprecipitation (MeDIP) followed by next-generation sequencing (MeDIP-seq). Canonical pathways, diseases and function and network analyses of the different samples were then performed using the Ingenuity
resultsTRAMP mice undergo extensive aberrant CpG hyper- and hypo-methylation. There were 2147 genes with a significant (log2-change ≥ 2) change in CpG methylation between the two groups, as mapped by the IPA software. Among these genes, the methylation of 1105 and 1042 genes was significantly decreased and increased, respectively, in TRAMP prostate tumors. The top associated disease identified by IPA was adenocarcinoma; however, the cAMP response element-binding protein (CREB)-, histone deacetylase 2 (HDAC2)-, glutathione S-transferase pi (GSTP1)- and polyubiquitin-C (UBC)-related pathways showed significantly altered methylation profiles based on the canonical pathway and network analyses. MSP and qPCR results of genes of interests corroborated with MeDIP-seq findings.
conclusionsThis is the first MeDIP-seq with IPA analysis of the TRAMP model to provide novel insight into the genome-wide methylation profile of prostate cancer. Studies on epigenetics, such as DNA methylation, will potentially provide novel avenues and strategies for further development of biomarkers targeted for treatment and prevention approaches for prostate cancer.
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