Inflammation as a Mediator of Microbiome Dysbiosis-Associated DNA Methylation Changes in Gastric Premalignant Lesions.

IF 3.7 Q2 GENETICS & HEREDITY Phenomics (Cham, Switzerland) Pub Date : 2023-09-06 eCollection Date: 2023-10-01 DOI:10.1007/s43657-023-00118-w

Lingjun Yan, Wanxin Li, Fenglin Chen, Junzhuo Wang, Jianshun Chen, Ying Chen, Weimin Ye

{"title":"Inflammation as a Mediator of Microbiome Dysbiosis-Associated DNA Methylation Changes in Gastric Premalignant Lesions.","authors":"Lingjun Yan, Wanxin Li, Fenglin Chen, Junzhuo Wang, Jianshun Chen, Ying Chen, Weimin Ye","doi":"10.1007/s43657-023-00118-w","DOIUrl":null,"url":null,"abstract":"Evidence for the influence of chronic inflammation induced by microbial dysbiosis on aberrant DNA methylation supports a plausible connexion between disordered microbiota and precancerous lesions of gastric cancer (PLGC). Here, a comprehensive study including multi-omics data was performed to estimate the relationships amongst the gastric microbiome, inflammatory proteins and DNA methylation alterations and their roles in PLGC development. The results demonstrated that gastric dysbacteriosis increased the risk of PLGC and DNA methylation alterations in related tumour suppressor genes. Seven inflammatory biomarkers were identified for antrum and corpus tissues, respectively, amongst which the expression levels of several biomarkers were significantly correlated with the microbial dysbiosis index (MDI) and methylation status of specific tumour suppressor genes. Notably, mediation analysis revealed that microbial dysbiosis partially contributed to DNA methylation changes in the stomach via the inflammatory cytokines C-C motif chemokine 20 (CCL20) and tumour necrosis factor receptor superfamily member 9 (TNFRSF9). Overall, these results may provide new insights into the mechanisms that might link the gastric microbiome to PLGC.Supplementary information: The online version contains supplementary material available at 10.1007/s43657-023-00118-w.","PeriodicalId":74435,"journal":{"name":"Phenomics (Cham, Switzerland)","volume":"3 5","pages":"496-501"},"PeriodicalIF":3.7000,"publicationDate":"2023-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10593640/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Phenomics (Cham, Switzerland)","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1007/s43657-023-00118-w","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2023/10/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"GENETICS & HEREDITY","Score":null,"Total":0}

引用次数: 0

Abstract

Evidence for the influence of chronic inflammation induced by microbial dysbiosis on aberrant DNA methylation supports a plausible connexion between disordered microbiota and precancerous lesions of gastric cancer (PLGC). Here, a comprehensive study including multi-omics data was performed to estimate the relationships amongst the gastric microbiome, inflammatory proteins and DNA methylation alterations and their roles in PLGC development. The results demonstrated that gastric dysbacteriosis increased the risk of PLGC and DNA methylation alterations in related tumour suppressor genes. Seven inflammatory biomarkers were identified for antrum and corpus tissues, respectively, amongst which the expression levels of several biomarkers were significantly correlated with the microbial dysbiosis index (MDI) and methylation status of specific tumour suppressor genes. Notably, mediation analysis revealed that microbial dysbiosis partially contributed to DNA methylation changes in the stomach via the inflammatory cytokines C-C motif chemokine 20 (CCL20) and tumour necrosis factor receptor superfamily member 9 (TNFRSF9). Overall, these results may provide new insights into the mechanisms that might link the gastric microbiome to PLGC.

Supplementary information: The online version contains supplementary material available at 10.1007/s43657-023-00118-w.

查看原文

微信好友朋友圈 QQ好友复制链接

本刊更多论文

炎症作为胃恶性前期病变中微生物组失调相关DNA甲基化变化的介导因子。

微生物微生态失调诱导的慢性炎症对异常DNA甲基化的影响的证据支持紊乱的微生物群与癌症癌前病变（PLGC）之间的可能联系。在这里，进行了一项包括多组学数据的综合研究，以评估胃微生物组、炎症蛋白和DNA甲基化改变之间的关系及其在PLGC发展中的作用。结果表明，胃菌群失调增加了相关肿瘤抑制基因PLGC和DNA甲基化改变的风险。胃窦和胃体组织分别鉴定了7种炎症生物标志物，其中几种生物标志物的表达水平与微生物微生态失调指数（MDI）和特定肿瘤抑制基因的甲基化状态显著相关。值得注意的是，中介分析显示，微生物微生态失调通过炎性细胞因子C-C基序趋化因子20（CCL20）和肿瘤坏死因子受体超家族成员9（TNFRSF9）部分促成了胃中DNA甲基化的变化。总的来说，这些结果可能会为胃微生物组与PLGC的联系机制提供新的见解。补充信息：在线版本包含补充材料，可访问10.1007/s43657-023-00118-w。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文去求助

来源期刊

Phenomics (Cham, Switzerland)

自引率

0.00%

发文量