METTL5 stabilizes c-Myc by facilitating USP5 translation to reprogram glucose metabolism and promote hepatocellular carcinoma progression.

Cancer communications (London, England)(2023)

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摘要
These findings point to a novel mechanism by which CREB1/P300-METTL5-USP5-c-Myc controls abnormal glucose metabolism and promotes tumor growth, suggesting that METTL5 is a potential therapeutic target and prognostic biomarker for HCC.
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关键词
CREB1,METTL5,P300,USP5,c-Myc,deubiquitination,glucose metabolism,hepatocellular carcinoma
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