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Primary inverse-variance weighting was complemented by sensitivity, heterogeneity, and horizontal pleiotropy assessments. The study highlights microbial taxa linked to increased or protective gastric cancer risk and identifies mediation involving inflammatory signaling.",{"@graph":14,"@context":73},[15,34,56],{"@type":16,"itemListElement":17},"BreadcrumbList",[18,23,27,31],{"item":19,"name":20,"@type":21,"position":22},"https://docshare.wps.com","Home","ListItem",1,{"item":24,"name":25,"@type":21,"position":26},"https://docshare.wps.com/document/","Document",2,{"item":28,"name":29,"@type":21,"position":30},"https://docshare.wps.com/document/healthcare/","Healthcare",3,{"item":32,"name":10,"@type":21,"position":33},"https://docshare.wps.com/document/gut-microbiota-influences-gastric-cancer-through-the-mediation-of-inflammatory-proteins-a-mendelian-randomization-analysis/360783/",4,{"url":32,"name":10,"@type":35,"image":36,"author":41,"headline":10,"publisher":44,"fileFormat":47,"inLanguage":8,"description":12,"dateModified":48,"datePublished":49,"encodingFormat":47,"isAccessibleForFree":50,"interactionStatistic":51},"DigitalDocument",{"url":37,"@type":38,"width":39,"height":40},"https://docshare.wps.com/thumbnails/gut-microbiota-influences-gastric-cancer-through-the-mediation-of-inflammatory-proteins-a-mendelian-randomization-analysis/360783.png","ImageObject",300,407,{"name":42,"@type":43},"Bulrr","Person",{"url":19,"name":45,"@type":46},"DocShare","Organization","application/pdf","2026-10-29","2026-09-23",true,{"@type":52,"interactionType":53,"userInteractionCount":55},"InteractionCounter",{"@type":54},"ViewAction",11,{"@type":57,"mainEntity":58},"FAQPage",[59,65,69],{"name":60,"@type":61,"acceptedAnswer":62},"What was the objective of this Mendelian randomization study?","Question",{"text":63,"@type":64},"To determine a cause-and-effect link between gastric cancer, gut microbiota, and inflammatory proteins using Mendelian randomization.","Answer",{"name":66,"@type":61,"acceptedAnswer":67},"How were the causal relationships assessed?",{"text":68,"@type":64},"Genome-wide association study data for intestinal microbiota, gastric cancer, and 91 inflammatory proteins were analyzed with Mendelian randomization, using inverse-variance weighting as the primary method plus sensitivity and pleiotropy checks.",{"name":70,"@type":61,"acceptedAnswer":71},"Which gut microbiota genus showed a mediating role in risk of gastric cancer?",{"text":72,"@type":64},"Genus Ruminococcaceae UCG014 may mediate increased risk of gastric cancer via downregulation of C-X-C motif chemokine 1, with a mediation ratio of 7.79%.","https://schema.org",{"og:url":32,"og:type":75,"og:title":10,"og:site_name":45,"og:description":12},"article",{"robots":77,"canonical":32},"index,follow",{"doc_id":79,"site_id":7},360783,1790176143,{"code":4,"msg":82,"data":83},"success",[84,88,92,96,101,106,110,115,120,123,127],{"id":22,"doc_module":4,"doc_module_name":25,"category_name":85,"show_sort_weight":86,"slug":87},"Story & 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Mendelian randomization analysis  \nChenyang Yu, MMa , Fule Wang, MMb , Xinfang Zhang, MMa , Wenzhao Guo, MMa , Changchuan Bai, MBc , Guanhua Lv, MDd ,*  \n\n| Abstract\u003Cbr>A robust correlation exists between gastric cancer (GC) and intestinal flora, potentially facilitated by inflammatory proteins. Nevertheless, the precise relationship between GC, intestinal flora, and their respective mediators remains unclear. The objective of this study is to employ a Mendelian randomization (MR) study to determine the cause-and-effect link between GC, inflammatory proteins, and gut microbiota. The genome-wide association study data pertaining to intestinal microbiota, GC, and 91 inflammatory proteins were obtained from a public database and subjected to MR analysis to ascertain the causal relationship between intestinal microbiota and GC. To evaluate the possible mediating function of latent inflammatory proteins in this process, a two-step MR study was used. Inverse-variance weighting was the primary analytical technique used; sensitivity, heterogeneity, and horizontal multiplicity studies were also carried out. Our MR analysis revealed potential associations between 11 bacterial genera in the gut microbiota and GC in Europeans, with 3 genera suggesting an increased risk and 8 a protective role. Among the inflammatory proteins, 3 demonstrated potential associations with GC, with 1 indicating a higher risk and 2 a protective effect. A two-step MR analysis indicated that genus Ruminococcaceae UCG014 may mediate an increased risk of GC through the downregulation of C-X-C motif chemokine 1, with a mediation ratio of 7.79% . The current research offers evidence that intestinal flora influences the risk of GC development through inflammatory proteins by means of MR analysis. The results of the MR analysis indicated that in European populations, certain microbial taxa may influence GC risk through C-X-C motif chemokine 1. |\n| --- |\n| Abbreviations: CCL19 = C-C motif chemokine 19 , CXCL1 = C-X-C motif chemokine 1 , GC = gastric cancer, GWAS = genomewide association study, IVs = instrumental variables, IVW = inverse-variance weighted, MR = Mendelian randomization, SNP = single-nucleotide polymorphism, TGF-alpha = transforming growth factor-alpha. |\n| Keywords: gastric cancer, gut microbiota, inflammatory proteins, Mendelian randomization |\n\n1. Introduction  \nThe global epidemiologic status of gastric cancer (GC) and the research advances made over the past few years have revealed several key trends and findings. Despite a decline in global incidence and mortality rates, GC remains the fourth greatest cause of cancer-related fatalities. [1] As indicated in Global Cancer Statistics 2020,[2] the number of new cases of GC  \nreached approximately 1.09 million in 2020, while the number of deaths was as high as 769,000 . [3] This underscores the significant global public health burden associated with this disease and highlights the formidable challenge in preventing and treating it effectively.  \nThe intestinal microbial community in the human body is a complex ecosystem comprising a multitude of microorganisms, with more than a thousand species, as evidenced by recent  \nCYand FW contributed to this article equally.  \nThis study was supported by the first batch of China Association of Traditional Chinese Medicine Joint Research Project in 2024 (project code:  \n2024DYPLHGG-03) and 2025 Liaoning Provincial Science and Technology Program – Joint Program (Natural Science Foundation – General Program, 2025-MSLH-399).  \nThe authors have no conflicts of interest to declare.  \nAll data generated or analyzed during this study are included in this published article (and its supplementary information files).  \nThis study is based on publicly available data and does not necessitate the signature of a written statement of understanding from the particip","cbCaihe3yiZGTIHz","https://ap.wps.com/l/cbCaihe3yiZGTIHz","pdf",3773927,"English","# Introduction\n## Study rationale and global burden\n## Gut microbiota and inflammatory proteins background\n## Mendelian randomization approach (overview)\n# Abstract\n## Objective and design\n## Data sources and analysis plan\n## Key findings and mediation results","[{\"question\":\"What was the objective of this Mendelian randomization study?\",\"answer\":\"To determine a cause-and-effect link between gastric cancer, gut microbiota, and inflammatory proteins using Mendelian randomization.\"},{\"question\":\"How were the causal relationships assessed?\",\"answer\":\"Genome-wide association study data for intestinal microbiota, gastric cancer, and 91 inflammatory proteins were analyzed with Mendelian randomization, using inverse-variance weighting as the primary method plus sensitivity and pleiotropy checks.\"},{\"question\":\"Which gut microbiota genus showed a mediating role in risk of gastric cancer?\",\"answer\":\"Genus Ruminococcaceae UCG014 may mediate increased risk of gastric cancer via downregulation of C-X-C motif chemokine 1, with a mediation ratio of 7.79%.\"}]","Gut microbiota influences gastric cancer through the mediation of inflammatory proteins - A Mendelian randomization analysis | PDF",1790141551]