ArticleJournal of advanced research2026
METTL4 enhances GLI1 translation through m
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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13 authors.
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Abstract
introductionHepatocellular carcinoma (HCC) is a major cause of cancer-related mortality. Epigenetic dysregulation, particularly through methyltransferase METTL4, plays a critical role in HCC progression. METTL4 is known to catalyze m
objectiveThis study aims to firstly investigate the role of METTL4 in the pathogenesis of HCC, and then to evaluate the antitumor efficacy of targeting METTL4 in inhibiting HCC growth and metastasis.
methodsIn a total of 802 postoperative HCC patients from four independent cohorts, we analyzed METTL4 expression in HCC tissues and its correlation with tumor staging and survival rates. Functional assays assessed the impact of METTL4 knockdown on HCC cell proliferation and metastasis, and patient-derived organoids (PDO) were used to evaluate the therapeutic efficacy of targeting METTL4. m
resultsMETTL4 was significantly upregulated in HCC tissues, correlating with higher tumor staging and poorer survival. Knockdown of METTL4 significantly inhibited HCC cell proliferation, migration, tumor growth, and lung metastasis. Meanwhile, targeting METTL4 effectively inhibited the growth of HCC PDO. METTL4-mediated m
conclusionsOur findings highlight the role of METTL4-mediated m
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