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• W4229021623 endingPage "413" @default.
• W4229021623 startingPage "395" @default.
• W4229021623 abstract "Arsenic is an environmental carcinogen. While not a direct mutagen, arsenic methylation during its elimination may stress cellular methyl donor pools, causing dysfunctional methylation and creating an epigenetic path to cancer. Here we performed differential methylation and transcriptomics, as well as genomic sequencing, in an in vitro transformation model, using human prostate cells. RWPE-1 prostate epithelial cells were transformed into malignant CAsE-PE cells after twenty-nine weeks of arsenic exposure in vitro. Our data showed increased expression of an activated KRAS oncogene, without its methylation being altered. Here we report 1,627 differentially methylated genes, but only 286 had altered expression, and just 157 showed an inverse relationship of methylation and expression. Identities and functions of such methylated, differentially expressed genes were not compelling markers—not compelling enough to drive transformation—by comparison with oncogenic KRAS. In this model, methylation-sponsored expression changes appear to be a consequence of oncogene-mediated cell signaling and transformation. Global genomic, transcriptional, and methylation sequencing are needed for improved insights into arsenic tumor formation." @default.
• W4229021623 created "2022-05-08" @default.
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• W4229021623 date "2022-04-27" @default.
• W4229021623 modified "2023-09-23" @default.
• W4229021623 title "Cause or Consequence" @default.
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• W4229021623 doi "https://doi.org/10.1002/9781119807704.ch18" @default.
• W4229021623 hasPublicationYear "2022" @default.
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