Helicobacter pylori Eradication Can Reverse the Methylation-Associated Regulation of miR-200a/b in Gastric Carcinogenesis
- Author:
Ji Min CHOI
1
;
Sang Gyun KIM
;
Hyo-Joon YANG
;
Joo Hyun LIM
;
Nam-Yun CHO
;
Woo Ho KIM
;
Joo Sung KIM
;
Hyun Chae JUNG
Author Information
- Publication Type:Original Article
- From:Gut and Liver 2020;14(5):571-580
- CountryRepublic of Korea
- Language:English
-
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.
