Gut Liver.
2020 Sep;14(5):571-580. 10.5009/gnl19299.
Helicobacter pylori Eradication Can Reverse the Methylation-Associated Regulation of miR-200a/b in Gastric Carcinogenesis
- Affiliations
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- 1Department of Internal Medicine, Healthcare Research Institute, Seoul National University Hospital Healthcare System Gangnam Center,Seoul, Korea
- 2Department of Internal Medicine and Liver Research Institute, Seoul National University College of Medicine, Seoul, Korea
- 3Department of Internal Medicine, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea
- 4Laboratory of Epigenetics, Cancer Research Institute, Seoul, Korea
- 5Department of Pathology, Seoul National University College of Medicine, Seoul, Korea
- KMID: 2506431
- DOI: http://doi.org/10.5009/gnl19299
Abstract
- Background/Aims
Epigenetic change is one of the mecha- nisms that regulates the expression of microRNAs (miRNAs) and is known to play a role in Helicobacter pylori-associated gastric carcinogenesis. We aimed to evaluate the epigen-etic changes ofmiR-200a/b in H. pylori-associated gastric carcinogenesis and restoration after eradication.
Methods
The expression and methylation levels of miR-200a/b were evaluated in gastric cancer (GC) cell lines, human gastric mu-cosa of H. pylori-negative and -positive controls, and H. pyloripositive GC patients. Next, the changes in the expression and methylation levels of miR-200a/b were compared between H. pylori-eradication and H. pylori-persistence groups at 6 months. Real-time reverse transcription-polymerase chain reaction was conducted to investigate the miRNA expression levels, and MethyLight was performed to assess the meth-ylation levels.
Results
In the GC cell lines, the level ofmiR-200a/b methylation decreased and the level of expression increased after demethylation. In the human gastric mucosa, the miR-200a/b methylation levels increased in the following group order: H. pylori-negative control group, H. pylori-positive control group, and H. pylori-positive GC group. Conversely, the miR-200a/b expression levels decreased in the same order. In the H. pylori-persistence group, no significant changes were observed in the methylation and expression levels of miR-200a/b after 6 months, whereas the level of methyla-tion decreased and the level of expression of miR-200a/b increased significantly 6 months in the H. pylori-eradication group.
Conclusions
Epigenetic alterations ofmiR-200a/bmay be implicated in H. pylori-induced gastric carcinogen-esis. This field defect for cancerization is suggested to be improved by H. pylori eradication.
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