• Medicine · Mar 2024

    The Role of Epstein-Barr Virus (EBV) Infected Gastric Cancer in Increasing microRNA124 (miR-124) Promoter Methylation and Enhancer of Zeste Homolog 2 (EZH2) Gene Expression.

    • Zohreh-Al-Sadat Ghoreshi, Rezaei Zadeh RukerdMohammadMUniversal Scientific Education and Research Network (USERN), Tehran, Iran., Hedyeh Askarpour, Ali Asghar Kheirkhah Vakilabad, Mohsen Nakhaie, Mohammad Javad Abbaszadeh Afshar, Emad Behboudi, Javad Charostad, and Nasir Arefinia.
    • School of Medicine, Jiroft University of Medical Sciences, Jiroft, Iran.
    • Medicine (Baltimore). 2024 Mar 22; 103 (12): e36534e36534.

    AbstractThe tumor suppressor microRNAs, miR-21, miR-124, and miR-494, participate in the controlling several cellular processes. To assess target miRNAs promoter methylation levels, we investigated 304 pairs of gastric cancer (GC) tissues and non-tumor tissues. We used a commercial real-time polymerase chain reaction (RT-PCR) for Epstein-Barr virus (EBV) and Helicobacter pylori kit to detect EBV and H. pylori DNA in GC tissues. After finding hypermethylation in the promoter of the miR-124 gene, we evaluated its expression level using quantitative PCR (qPCR). Bioinformatics analysis confirmed miR-124 as a target of enhancer of Zeste homolog 2 (EZH2). Additionally, qPCR confirmed the association between EZH2 and miR-124. EBV and H. pylori DNA were detected in 9.5% and 15.1% of GC patients, respectively. Our findings also revealed significant differences in the miR-124 methylation levels among EBV-infected GC patients, H. pylori infected GC patients, GC patients without EBV and H. pylori infection, and non-tumor tissue. Bioinformatics and qPCR assays suggested an inverse relationship between the expression levels of EZH2 and miR-124 in EBV-infected GC patients. Our data revealed hypermethylation of the miR-124 promoter and significant reduction in its expression in EBV-infected GC tissues. It is possible that miR-124 may target EZH2 by binding to the 3'-UTR of the EZH2 gene, thus potentially contributing to the development of EBV-infected GC.Copyright © 2024 the Author(s). Published by Wolters Kluwer Health, Inc.

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