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Oncogenomic disruptions in arsenic-induced carcinogenesis

Adam P Sage1, Brenda C Minatel1, Kevin W Ng1

  • 1Department of Integrative Oncology, British Columbia Cancer Research Centre, Vancouver, British Columbia, Canada.

Oncotarget
|February 10, 2017
PubMed

Insights

Chronic arsenic exposure causes cancer by altering DNA and gene regulation. Arsenic biotransformation impacts genetic and epigenetic processes, leading to oncogenomic anomalies and the disruption of non-coding RNAs.

Area of Science:

  • Environmental Health
  • Molecular Biology
  • Cancer Research

Background:

  • Chronic arsenic exposure affects over 200 million people globally.
  • Arsenic exposure is linked to various cancers and adverse health outcomes.
  • Arsenic biotransformation is implicated in arsenic-induced carcinogenesis.

Purpose of the Study:

  • To provide an overview of oncogenomic anomalies associated with arsenic exposure.
  • To highlight the role of non-coding RNAs in arsenic-induced carcinogenesis.

Main Methods:

  • Review of existing literature on arsenic's effects on genetic and epigenetic levels.
  • Analysis of how arsenic biotransformation influences DNA integrity and gene expression.
  • Examination of the role of non-coding RNAs in arsenic-induced cancer.

Main Results:

  • Arsenic exposure causes genetic alterations, including DNA damage-repair interference and genomic instability.
  • Arsenic exposure leads to epigenetic changes, such as global hypomethylation and promoter-specific hypermethylation.
  • Deregulation of oncogenic and tumor-suppressive genes occurs due to arsenic-associated DNA alterations.
  • Aberrant non-coding RNA expression disrupts signaling pathways, contributing to arsenic-induced carcinogenesis.

Conclusions:

  • Arsenic exposure induces significant oncogenomic anomalies.
  • Non-coding RNAs play a critical role in the carcinogenic process initiated by arsenic exposure.
Keywords:
arseniccancerepigeneticsgeneticsnon-coding RNA

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