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Epigenome-wide DNA methylation profiling of periprostatic adipose tissue in prostate cancer patients with excess adiposity-a pilot study

2018-04-17Journal article Open access
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dc.contributor.authorCheng, Y.
dc.contributor.authorMonteiro, C.
dc.contributor.authorMatos, A.
dc.contributor.authorYou, J.
dc.contributor.authorFraga, A.
dc.contributor.authorPereira, C.
dc.contributor.authorCatalán, V.
dc.contributor.authorRodríguez, A.
dc.contributor.authorGómez-Ambrosi, J.
dc.contributor.authorFrühbeck, G.
dc.contributor.authorRibeiro, R.
dc.contributor.authorHu, P.
dc.date.accessioned2019-07-18T15:27:20Z
dc.date.available2019-07-18T15:27:20Z
dc.date.issued2018-04-17
dc.description.abstractBackground: Periprostatic adipose tissue (PPAT) has been recognized to associate with prostate cancer (PCa) aggressiveness and progression. Here, we sought to investigate whether excess adiposity modulates the methylome of PPAT in PCa patients. DNA methylation profiling was performed in PPAT from obese/overweight (OB/OW, BMI > 25 kg m-2) and normal weight (NW, BMI < 25 kg m-2) PCa patients. Significant differences in methylated CpGs between OB/OW and NW groups were inferred by statistical modeling. Results: Five thousand five hundred twenty-six differentially methylated CpGs were identified between OB/OW and NW PCa patients with 90.2% hypermethylated. Four hundred eighty-three of these CpGs were found to be located at both promoters and CpG islands, whereas the representing 412 genes were found to be involved in pluripotency of stem cells, fatty acid metabolism, and many other biological processes; 14 of these genes, particularly FADS1, MOGAT1, and PCYT2, with promoter hypermethylation presented with significantly decreased gene expression in matched samples. Additionally, 38 genes were correlated with antigen processing and presentation of endogenous antigen via MHC class I, which might result in fatty acid accumulation in PPAT and tumor immune evasion. Conclusions: Results showed that the whole epigenome methylation profiles of PPAT were significantly different in OB/OW compared to normal weight PCa patients. The epigenetic variation associated with excess adiposity likely resulted in altered lipid metabolism and immune dysregulation, contributing towards unfavorable PCa microenvironment, thus warranting further validation studies in larger samples.pt_PT
dc.description.sponsorshipThis work was supported in part by the Natural Sciences and Engineering Research Council of Canada, Manitoba Research Health Council, University of Manitoba, and China Scholarship Councilpt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationClin Epigenetics. 2018 Apr 17;10:54pt_PT
dc.identifier.doi10.1186/s13148-018-0490-3pt_PT
dc.identifier.issn1868-7075
dc.identifier.issn1868-7083
dc.identifier.urihttp://hdl.handle.net/10400.16/2279
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherBMCpt_PT
dc.relation.publisherversionhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5904983/pt_PT
dc.subjectDNA methylationpt_PT
dc.subjectMicroenvironmentpt_PT
dc.subjectObesitypt_PT
dc.subjectPeriprostatic adipose tissuept_PT
dc.subjectProstate cancerpt_PT
dc.titleEpigenome-wide DNA methylation profiling of periprostatic adipose tissue in prostate cancer patients with excess adiposity-a pilot studypt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.conferencePlaceGermanypt_PT
oaire.citation.issue1pt_PT
oaire.citation.startPage54pt_PT
oaire.citation.titleClinical Epigeneticspt_PT
oaire.citation.volume10pt_PT
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT

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