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While genetic contributors to GC have been extensively studied, the functional role of N6-methyladenosine (m6A) RNA methylation\u2014the most abundant eukaryotic RNA modification\u2014in gastric carcinogenesis remains insufficiently characterized. This study aimed to investigate transcriptome-wide m6A methylation dysregulation and its mechanistic implications in GC progression.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Methods<\/jats:title>\n            <jats:p>Methylated RNA immunoprecipitation sequencing (MeRIP-seq) was performed to map m6A epitranscriptomes in paired GC and adjacent normal tissues. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were conducted on 253 hypomethylated mRNAs to delineate the biological pathways associated with m6A dysregulation. The transcriptomic profiles were analyzed using RNA-seq, while a retrospective cohort analysis (<jats:italic>n\u2009=<\/jats:italic>\u200958) evaluated the correlations between <jats:italic>IGF2BP3<\/jats:italic> expression and the clinicopathological characteristics of patients with GC.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results<\/jats:title>\n            <jats:p>MeRIP-seq analysis demonstrated transcriptome-wide m6A hypomethylation in GC tissues, identifying 271 significantly reduced peaks (<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.01). Functional annotation revealed enrichment of hypomethylated transcripts in metabolic pathways and transcriptional dysregulation. Notably, m6A-related genes exhibited widespread activation in GC, with <jats:italic>IGF2BP3<\/jats:italic> showing the most pronounced upregulation (106-fold increase, <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.0001). Clinically, elevated <jats:italic>IGF2BP3<\/jats:italic> expression significantly correlated with lymph node involvement (<jats:italic>p<\/jats:italic>\u2009=\u20090.016) and advanced TNM staging (<jats:italic>p<\/jats:italic>\u2009=\u20090.028).<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusion<\/jats:title>\n            <jats:p>This study establishes m6A methylation dysregulation as a critical mechanism in GC pathogenesis and identifies <jats:italic>IGF2BP3<\/jats:italic> as both a potential therapeutic target and a prognostic biomarker in GC.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1186\/s40246-025-00802-0","type":"journal-article","created":{"date-parts":[[2025,8,22]],"date-time":"2025-08-22T18:00:17Z","timestamp":1755885617000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Clinical and prognostic significance of m6A hypomethylation and IGF2BP3 overexpression in gastric cancer: an integrated epigenomic-transcriptomic analysis"],"prefix":"10.1186","volume":"19","author":[{"given":"Xiangchen","family":"Hu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhe","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Youwei","family":"Kou","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yujing","family":"Huang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2025,8,22]]},"reference":[{"issue":"2","key":"802_CR1","doi-asserted-by":"publisher","first-page":"108","DOI":"10.1016\/j.tig.2012.11.003","volume":"29","author":"G Jia","year":"2013","unstructured":"Jia G, Fu Y, He C. 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