{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,29]],"date-time":"2026-10-29T23:23:52Z","timestamp":1793316232055,"version":"4.5.0"},"reference-count":293,"publisher":"Bioscientifica","issue":"2","content-domain":{"domain":["jme.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2023,2,1]]},"abstract":"<jats:p>Epitranscriptomic modification of RNA regulates human development, health, and disease. The true diversity of the transcriptome in breast cancer including chemical modification of transcribed RNA (epitranscriptomics) is not well understood due to limitations of technology and bioinformatic analysis. N-6-methyladenosine (m6A) is the most abundant epitranscriptomic modification of mRNA and regulates splicing, stability, translation, and intracellular localization of transcripts depending on m6A association with reader RNA-binding proteins. m6A methylation is catalyzed by the METTL3 complex and removed by specific m6A demethylase ALKBH5, with the role of FTO as an \u2018eraser\u2019 uncertain. In this review, we provide an overview of epitranscriptomics related to mRNA and focus on m6A in mRNA and its detection. We summarize current knowledge on altered levels of writers, readers, and erasers of m6A and their roles in breast cancer and their association with prognosis. We summarize studies identifying m6A peaks and sites in genes in breast cancer cells.<\/jats:p>","DOI":"10.1530\/jme-22-0110","type":"journal-article","created":{"date-parts":[[2022,11,11]],"date-time":"2022-11-11T06:51:55Z","timestamp":1668149515000},"update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-6","source":"Crossref","is-referenced-by-count":68,"title":["m6A readers, writers, erasers, and the m6A epitranscriptome in breast cancer"],"prefix":"10.1530","volume":"70","author":[{"given":"Belinda J","family":"Petri","sequence":"first","affiliation":[{"name":"Department of Biochemistry & Molecular Genetics, University of Louisville School of Medicine, Louisville, Kentucky, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3358-4378","authenticated-orcid":true,"given":"Carolyn M","family":"Klinge","sequence":"additional","affiliation":[{"name":"Department of Biochemistry & Molecular Genetics, University of Louisville School of Medicine, Louisville, Kentucky, USA"},{"name":"University of Louisville Center for Integrative Environmental Health Sciences (CIEHS), Louisvillle, Kentucky, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"416","reference":[{"key":"bib1","series-title":"Molecular and Cellular Biology","article-title":"SRC increases MYC mRNA expression in estrogen receptor-positive breast cancer via mRNA stabilization and inhibition of p53 function","volume":"38","author":"Abdullah","year":"2018","unstructured":"Abdullah CKorkaya HIizuka SCourtneidge SA2018SRC increases MYC mRNA expression in estrogen receptor-positive breast cancer via mRNA stabilization and inhibition of p53 function. 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