Please use this identifier to cite or link to this item: https://doi.org/10.1038/srep40569
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dc.titleDietary phytochemical PEITC restricts tumor development via modulation of epigenetic writers and erasers
dc.contributor.authorPark, J.E
dc.contributor.authorSun, Y
dc.contributor.authorLim, S.K
dc.contributor.authorTam, J.P
dc.contributor.authorDekker, M
dc.contributor.authorChen, H
dc.contributor.authorSze, S.K
dc.date.accessioned2020-10-21T08:04:08Z
dc.date.available2020-10-21T08:04:08Z
dc.date.issued2017
dc.identifier.citationPark, J.E, Sun, Y, Lim, S.K, Tam, J.P, Dekker, M, Chen, H, Sze, S.K (2017). Dietary phytochemical PEITC restricts tumor development via modulation of epigenetic writers and erasers. Scientific Reports 7 : 40569. ScholarBank@NUS Repository. https://doi.org/10.1038/srep40569
dc.identifier.issn20452322
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/178710
dc.description.abstractDietary intake of bioactive phytochemicals including the cruciferous vegetable derivative phenethyl isothiocyanate (PEITC) can reduce risk of human cancers, but possible epigenetic mechanisms of these effects are yet unknown. We therefore sought to identify the molecular basis of PEITC-mediated epigenetic tumor restriction. Colon cancer cells treated with low-dose PEITC for >1 month exhibited stable alterations in expression profile of epigenetic writers/erasers and chromatin-binding of histone deacetylases (HDACs) and Polycomb-group (PcG) proteins. Sustained PEITC exposure not only blocked HDAC binding to euchromatin but was also associated with hypomethylation of PcG target genes that are typically hypermethylated in cancer. Furthermore, PEITC treatment induced expression of pro-Apoptotic genes in tumor cells, which was partially reversed by overexpression of PcG member BMI-1, suggesting opposing roles for PEITC and PcG proteins in control of tumor progression. These data demonstrate that PEITC regulates chromatin binding of key epigenetic writers/erasers and PcG complexes to restrict tumor development. © The Author(s) 2017.
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceUnpaywall 20201031
dc.subjectBIM protein
dc.subjecthistone
dc.subjectisothiocyanic acid derivative
dc.subjectphenethyl isothiocyanate
dc.subjectphytochemical
dc.subjectpolycomb group protein
dc.subjectanimal
dc.subjectapoptosis
dc.subjectcarcinogenesis
dc.subjectcolon tumor
dc.subjectdiet
dc.subjectDNA methylation
dc.subjectdown regulation
dc.subjectdrug effect
dc.subjectgene expression regulation
dc.subjectgene ontology
dc.subjectgenetic epigenesis
dc.subjectgenetics
dc.subjectmetabolism
dc.subjectnude mouse
dc.subjectpathology
dc.subjectphenotype
dc.subjecttime factor
dc.subjecttumor cell line
dc.subjectupregulation
dc.subjectAnimals
dc.subjectApoptosis
dc.subjectBcl-2-Like Protein 11
dc.subjectCarcinogenesis
dc.subjectCell Line, Tumor
dc.subjectColonic Neoplasms
dc.subjectDiet
dc.subjectDNA Methylation
dc.subjectDown-Regulation
dc.subjectEpigenesis, Genetic
dc.subjectGene Expression Regulation, Neoplastic
dc.subjectGene Ontology
dc.subjectHistones
dc.subjectIsothiocyanates
dc.subjectMice, Nude
dc.subjectPhenotype
dc.subjectPhytochemicals
dc.subjectPolycomb-Group Proteins
dc.subjectTime Factors
dc.subjectUp-Regulation
dc.typeArticle
dc.contributor.departmentDEPT OF SURGERY
dc.description.doi10.1038/srep40569
dc.description.sourcetitleScientific Reports
dc.description.volume7
dc.description.page40569
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