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논문 기본 정보

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학술저널
저자정보
Ji Min Choi (Department of Internal Medicine Healthcare Research Institute Seoul National University Hospital He) Sang Gyun Kim (Department of Internal Medicine and Liver Research Institute Seoul National University College of M) Hyo-Joon Yang (Department of Internal Medicine Kangbuk Samsung Hospital Sungkyunkwan University School of Medicine) Joo Hyun Lim (Department of Internal Medicine Healthcare Research Institute Seoul National University Hospital He) Nam-Yun Cho (Laboratory of Epigenetics Cancer Research Institute Seoul National University College of Medicine S) Woo Ho Kim (Department of Pathology Seoul National University College of Medicine Seoul Korea) Joo Sung Kim (Department of Internal Medicine Healthcare Research Institute Seoul National University Hospital He) Hyun Chae Jung (Department of Internal Medicine and Liver Research Institute Seoul National University College of M)
저널정보
거트앤리버 발행위원회 Gut and Liver Gut and Liver 제14권 제5호
발행연도
2020.1
수록면
571 - 580 (10page)

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Background/Aims: Epigenetic change is one of the mechanisms 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 epigenetic changes of miR-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 mucosa 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 methylation levels. Results: In the GC cell lines, the level of miR- 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 methylation decreased and the level of expression of miR-200a/b increased significantly 6 months in the H. pylori-eradication group. Conclusions: Epigenetic alterations of miR-200a/b may be implicated in H. pylori -induced gastric carcinogenesis. This field defect for cancerization is suggested to be improved by H. pylori eradication.

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