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Table 1 Effects of metabolites on post-translational modification of EZH2 protein

From: Symphony of epigenetic and metabolic regulation—interaction between the histone methyltransferase EZH2 and metabolism of tumor

Type Modification enzyme Site Biological Functions Metabolites Metabolic pathways Ref.
Phosphorylation AMPK T311 Disrupts EZH2 interaction with SUZ12, suppresses PRC2 HMTase activity and releases target genes (OLIG2, SOX17, GATA6), resulting in cell cycle arrest and cell differentiation ATP Glucose metabolism (glycolysis, etc.) [78]
AKT S21 Suppresses EZH2 HMTase activity and releases target genes (HOXA9), promoting tumor progression ATP Energy metabolism [79]
S21 Inhbits EZH2 HMTase activity and releases target genes (IGF1, BCL2, HIF1A), leading to the MM cell drug resistance ATP Energy metabolism [83]
S21 Activates EZH2 as a coactivator for critical transcription factors including the androgen receptor, promoting tumor cells growth ATP Energy metabolism [31]
S21 Facilitates EZH2-mediated STAT3 methylation and enhances EZH2-STAT3 interaction and STAT3 activity, which accelerates GSC self-renewal and glioblastoma tumor process ATP Energy metabolism [28]
Acetylation PCAF K348 Enhances EZH2 stability and function and the migration and invasion ability of lung cancer Acetyl-CoA Fatty acid β-oxidation, TCA cycle, pyruvate and acetate metabolism [94]
O-GlcNAcylation OGT S75 Enhances EZH2 stability and function, contributing to tumorigenesis UDP-GlcNAc Glucose, amino acids, fatty acids and nucleotide metabolism [98]
S73, S76, S84, T313, S729 Enhance EZH2 stability and function, promoting cancer progression [99]
—— Promotes the migration and invasion of advanced colorectal cancer by enhancing EZH2 stability and activity [100]