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Journal of Cancer Prevention

Review

Journal of Cancer Prevention 2014; 19(4): 259-264

Published online December 31, 2014

https://doi.org/10.15430/JCP.2014.19.4.259

© Korean Society of Cancer Prevention

Helicobacter pylori Induces Hypermethylation of CpG Islands Through Upregulation of DNA Methyltransferase: Possible Involvement of Reactive Oxygen/Nitrogen Species

Hye-Kyung Na, and Jeong-Hwa Woo

Department of Food and Nutrition, College of Human Ecology, Sungshin Women’s University, Seoul, Korea

Correspondence to :
Hye-Kyung Na, Department of Food and Nutrition, College of Human Ecology, Sungshin Women’s University, 55 Dobong-ro 76ga-gil, Gangbuk-gu, Seoul 142-732, Korea, Tel: +82-2-920-7688, Fax: +82-2-920-2076, E-mail: nhkdec28@gmail.com

Received: December 22, 2014; Accepted: December 24, 2014

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Helicobacter pylori infection has been considered to be one of the major factors implicated in etiology of gastric cancer. Aberrant DNA methylation accounts for epigenetic modifications induced by H. pylori. H. pylori-induced hypermethylation has been linked to enhancement of the rates of metastasis and recurrence in gastric cancer patients. H. pylori-induced gene hypermethylation has been known to be associated with inflammation. However, the molecular mechanisms underlying H. pylori-induced hypermethylation remain largely unknown. This review highlights possible involvement of reactive oxygen/nitrogen species in H. pylori-induced hypermethylation and gastric carcinogenesis.

Keywords: Helicobacter pylori, Hypermethylation, Reactive oxygen species, Reactive nitrogen species, Gastric cancer

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