Molecular mechanisms of H. Pylori-induced DNA double-strand breaks

Research output: Contribution to journalReview article

3 Citations (Scopus)

Abstract

Infections contribute to carcinogenesis through inflammation-related mechanisms. H. pylori infection is a significant risk factor for gastric carcinogenesis. However, the molecular mechanism by which H. pylori infection contributes to carcinogenesis has not been fully elucidated. H. pylori-associated chronic inflammation is linked to genomic instability via reactive oxygen and nitrogen species (RONS). In this article, we summarize the current knowledge of H. pylori-induced double strand breaks (DSBs). Furthermore, we provide mechanistic insight into how processing of oxidative DNA damage via base excision repair (BER) leads to DSBs. We review recent studies on how H. pylori infection triggers NF-κB/inducible NO synthase (iNOS) versus NF-κB/nucleotide excision repair (NER) axis-mediated DSBs to drive genomic instability. This review discusses current research findings that are related to mechanisms of DSBs and repair during H. pylori infection.

Original languageEnglish (US)
Article number2891
JournalInternational journal of molecular sciences
Volume19
Issue number10
DOIs
StatePublished - Oct 2018

Fingerprint

Double-Stranded DNA Breaks
Pylorus
infectious diseases
strands
DNA
Repair
deoxyribonucleic acid
Reactive Nitrogen Species
Infection
Carcinogenesis
Genomic Instability
Nucleotides
Nitric Oxide Synthase
DNA Repair
Reactive Oxygen Species
Inflammation
Nitrogen
nucleotides
Oxygen
Processing

Keywords

  • BER
  • DSBs
  • H.Pylori
  • NER
  • NF-κB
  • RONS

ASJC Scopus subject areas

  • Catalysis
  • Molecular Biology
  • Spectroscopy
  • Computer Science Applications
  • Physical and Theoretical Chemistry
  • Organic Chemistry
  • Inorganic Chemistry

Cite this

Molecular mechanisms of H. Pylori-induced DNA double-strand breaks. / Kidane, Dawit.

In: International journal of molecular sciences, Vol. 19, No. 10, 2891, 10.2018.

Research output: Contribution to journalReview article

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AB - Infections contribute to carcinogenesis through inflammation-related mechanisms. H. pylori infection is a significant risk factor for gastric carcinogenesis. However, the molecular mechanism by which H. pylori infection contributes to carcinogenesis has not been fully elucidated. H. pylori-associated chronic inflammation is linked to genomic instability via reactive oxygen and nitrogen species (RONS). In this article, we summarize the current knowledge of H. pylori-induced double strand breaks (DSBs). Furthermore, we provide mechanistic insight into how processing of oxidative DNA damage via base excision repair (BER) leads to DSBs. We review recent studies on how H. pylori infection triggers NF-κB/inducible NO synthase (iNOS) versus NF-κB/nucleotide excision repair (NER) axis-mediated DSBs to drive genomic instability. This review discusses current research findings that are related to mechanisms of DSBs and repair during H. pylori infection.

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