Gastric cancer: Epigenetic mechanisms: Aberrant DNA methylation and dysregulation of microRNA

Research output: Chapter in Book/Report/Conference proceedingChapter

1 Citation (Scopus)

Abstract

Like many human cancers, global DNA hypomethylation and promoter CpG island hypermethylation in tumor suppressor or tumor-related genes are frequently observed in gastric cancer, and aberrant DNA methylation occurs in a gene-specific manner during the multistep gastric carcinogenesis. Chronic Helicobacter pylori (H. pylori) infection induces proinflammatory cytokines and reactive oxygen and nitrogen species in the gastric mucosa, which is known to be associated with the accumulation of aberrant DNA methylation. Aberrant DNA methylation caused by H. pylori-associated gastritis persists even after the disappearance of H. pylori, and epigenetic alterations induced by H. pylori correlate with the risk for gastric cancer. Numerous microRNAs (miRNAs) are dysregulated during the gastric carcinogenesis, and some of these miRNAs are known to be also dysregulated by H. pylori infection. miRNAs dysregulated by H. pylori infection play an important role in gastric carcinogenesis by modulating inflammation and immune response of the host, cell cycle progression, apoptosis and proliferation, and tumor invasion and metastasis.

Original languageEnglish
Title of host publicationHelicobacter pylori
PublisherSpringer Singapore
Pages257-267
Number of pages11
ISBN (Electronic)9789812877062
ISBN (Print)9789812877055
DOIs
StatePublished - 16 Jun 2016

Fingerprint

DNA Methylation
MicroRNAs
Epigenomics
Helicobacter pylori
Stomach Neoplasms
Helicobacter Infections
Stomach
Carcinogenesis
Neoplasms
Reactive Nitrogen Species
CpG Islands
Gastritis
Gastric Mucosa
Genes
Reactive Oxygen Species
Cell Cycle
Cell Proliferation
Apoptosis
Cytokines
Neoplasm Metastasis

Keywords

  • Epigenetics
  • Gastric cancer
  • Helicobacter pylori
  • Methylation
  • MicroRNA

Cite this

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abstract = "Like many human cancers, global DNA hypomethylation and promoter CpG island hypermethylation in tumor suppressor or tumor-related genes are frequently observed in gastric cancer, and aberrant DNA methylation occurs in a gene-specific manner during the multistep gastric carcinogenesis. Chronic Helicobacter pylori (H. pylori) infection induces proinflammatory cytokines and reactive oxygen and nitrogen species in the gastric mucosa, which is known to be associated with the accumulation of aberrant DNA methylation. Aberrant DNA methylation caused by H. pylori-associated gastritis persists even after the disappearance of H. pylori, and epigenetic alterations induced by H. pylori correlate with the risk for gastric cancer. Numerous microRNAs (miRNAs) are dysregulated during the gastric carcinogenesis, and some of these miRNAs are known to be also dysregulated by H. pylori infection. miRNAs dysregulated by H. pylori infection play an important role in gastric carcinogenesis by modulating inflammation and immune response of the host, cell cycle progression, apoptosis and proliferation, and tumor invasion and metastasis.",
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Gastric cancer : Epigenetic mechanisms: Aberrant DNA methylation and dysregulation of microRNA. / Shin, Cheol Min.

Helicobacter pylori. Springer Singapore, 2016. p. 257-267.

Research output: Chapter in Book/Report/Conference proceedingChapter

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