Epigenetic targets of arsenic: Emphasis on epigenetic modifications during carcinogenesis

Ram Vinod Roy, Young Ok Son, Poyil Pratheeshkumar, Lei Wang, John Andrew Hitron, Sasidharan Padmaja Divya, D. Rakesh, Donghern Kim, Yuanqin Yin, Zhuo Zhang, Xianglin Shi

Research output: Contribution to journalArticlepeer-review

23 Scopus citations

Abstract

DNA methylation and histone modification promote opening and closure of chromatin structure, which affects gene expression without altering the DNA sequence. Epigenetic markers regulate the dynamic nature of chromatin structure at different levels: DNA, histone, noncoding RNAs, as well as the higher-order chromatin structure. Accumulating evidence strongly suggests that arsenic-induced carcinogenesis involves frequent changes in the epigenetic marker. However, progress in identifying arsenic-induced epigenetic changes has already been made using genome-wide approaches; the biological significance of these epigenetic changes remains unknown. Moreover, arsenic-induced changes in the chromatin state alter gene expression through the epigenetic mechanism. The current review provides a summary of recent literature regarding epigenetic changes caused by arsenic in carcinogenesis. We highlight the transgenerational studies needed to explicate the biological significance and toxicity of arsenic over a broad spectrum.

Original languageEnglish
Pages (from-to)63-84
Number of pages22
JournalJournal of Environmental Pathology, Toxicology and Oncology
Volume34
Issue number1
DOIs
StatePublished - 2015

Bibliographical note

Publisher Copyright:
© 2015 by Begell House, Inc.

Keywords

  • Arsenic
  • Carcinogenesis
  • Chromatin
  • DNA methylation
  • Epigenetics
  • Epigenome
  • Histone modification
  • Intergeneration
  • MiRNAs
  • Prenatal exposure
  • Transgenerational

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Toxicology
  • Health, Toxicology and Mutagenesis

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