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MicroRNAs (miRNAs) are currently considered as crucial post-transcriptional regulators of gene expression. Their roles in development, cell proliferation and differentiation are widely recognized. Furthermore, miRNAs are frequently altered in cancer cells and reveal their functions as either oncogenes or tumor suppressors. The emerging role of miRNAs in diverse and fundamental cellular mechanisms suggests that proper control of these regulatory elements is essential for the maintenance of a nonpathological state. Recent reports have highlighted the regulatory role of miRNAs in Helicobacter pylori infection and associated diseases. For example, a strong inflammatory response characterized by the early production of proinflammatory tumor necrosis factor (TNF)-α and interleukin (IL)-6 cytokines, followed by IL-10, IL-1β and IL-23 secretion as a consequence of miR-146a up-regulation and strong miR-155 induction, which raised the TNF-α production. In contrast, IL8, TNF-α and IL-1β could contribute to the induction of miR146a during H. pylori infection. Therefore, miRNAs modulate the H. pylori infection and are also affected by these bacteria, as, for example, the synthesis of the transcription factor nuclear factor-κB that can act as a transactivator of miR-200b and miR200c. Similarly, epigenetic change is one of the mechanisms that regulates the expression of miRNAs and has been known to play a role in H. pylori-associated gastric carcinogenesis. From this background Choi et al. aimed to evaluate the epigenetic changes of miR-200a/b in H. pylori-associated gastric carcinogenesis and whether H. pylori eradication restore epigenetic changes of miR-200a/b. The miR-200 family is closely linked to the expression of ZEB1 and ZEB2, key regulators of epithelialmesenchymal transition (EMT), and regulates crucial processes in carcinogenesis, such as tumor initiation, progression, invasion, and metastasis of various types of cancer. Recent studies have shown that miR-200 family were downregulated in gastric cancer (GC), suggesting its role as a tumor suppressor in GC. In addition, hypermethylation of the promoter CpG island was one of the mechanisms of miR-200c/141 downregulation. However, it has not yet been fully elucidated whether epigenetic alterations in the miR-200 family are affected by H. pylori infection and/or by its eradication. Choi et al. evaluated the expression and methylation levels of miR-200a/b in GC cell lines, human gastric mucosa of H. pylori-negative and -positive controls, and H. pyloripositive GC patients. They found that the level of miR200a/b methylation decreased and the level of expression increased after demethylation. Furthermore, the miR-200a/b methylation levels in the human gastric mucosa, increased in the order from H. pylori-negative control group, H. pylori-positive control group, and H. pylori-positive GC group. Interestingly the level of methylation decreased and the level of expression of miR-200a/b increased significantly only after 6 months in the H. pylori-eradicated group. These results suggest that epigenetic alterations of miR200a/b may be implicated in H. pylori-induced gastric carcinogenesis and H. pylori eradication improved the field defect for cancerization. The causal association between H. pylori infection and GC has been firmly established by many epidemiological and clinical studies. Although GC develops in approximately 1% to 3%

gut and liver

Reversal of the Methylation-Associated Regulation of miR-200a/b by &lt;i&gt;Helicobacter pylori&lt;/i&gt; Eradication Contributes to the Chemoprevention of Gastric Carcinogenesis