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Adv."],"published-print":{"date-parts":[[2026,9,11]]},"abstract":"<jats:p>\n                    Hepatocellular carcinoma (HCC) originates from premalignant disease-associated hepatocytes (daHeps) that emerge during the progression of metabolic dysfunction\u2013associated steatotic liver disease (MASLD) to metabolic dysfunction\u2013associated steatohepatitis (MASH). As daHeps are compensatorily primed by metabolic stress, we reproduced the accelerated progression of MASLD-associated HCC in mice by phenocopying the decreased expression of a metabolic regulator, protein arginine methyltransferase 1 (PRMT1). In\n                    <jats:italic toggle=\"yes\">Prmt1<\/jats:italic>\n                    liver-specific knockout (LKO), m\n                    <jats:sup>6<\/jats:sup>\n                    A-mediated changes in mRNA stability reprogram the transcriptome via paralog compensation; increased PRMT6 activates m\n                    <jats:sup>6<\/jats:sup>\n                    A methyltransferases by inducing asymmetric arginine dimethylation of METTL3. This event enhances global m\n                    <jats:sup>6<\/jats:sup>\n                    A deposition that leads to the down-regulation of\n                    <jats:italic toggle=\"yes\">Keap1<\/jats:italic>\n                    , which would trigger the NRF2 axis, promoting premalignancy; under diet- and chemical-induced stress, the incidence of steatohepatitic HCC was increased, clinically correlating with the PRMT-METTL3-NRF2 pathway. Together, we propose that compensatory arginine methylation primes MASLD-associated HCC by modulating m\n                    <jats:sup>6<\/jats:sup>\n                    A-mediated transcriptome and NRF2 regulatory pathways as adaptive defenses against metabolic and oxidative stress.\n                  <\/jats:p>","DOI":"10.1126\/sciadv.aec5094","type":"journal-article","created":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T17:58:47Z","timestamp":1788976727000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":0,"title":["Dysregulated m\n                    <sup>6<\/sup>\n                    A via compensatory arginine methylation primes premalignancy in metabolic dysfunction\u2013associated steatotic liver disease"],"prefix":"10.1126","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0161-6707","authenticated-orcid":true,"given":"Geun-Woo D.","family":"Kim","sequence":"first","affiliation":[{"name":"Division 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