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In colorectal cancer, phosphorylation by the tyrosine kinase Src and subsequent degradation of the differentiation-promoting P1-HNF4α led to the attenuation of its anti-cancer properties [14]

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3.1.2 Mechanisms of cuproptosis regulation in KOA In chondrocyte injury, dysregulated copper homeostasis leads to intracellular copper accumulation, which triggers cuproptosis via dual mechanisms: (i) direct binding to lipoylated TCA cycle enzymes (e.g., DLAT, PDHA1), inducing protein aggregation, mitochondrial respiratory dysfunction, and energy metabolism collapse