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In malignancy, this constitutes a constitutive, irreversible metabolic adaptation driven by oncogenic signaling (e.g., HIF-1 stabilization, c-Myc amplification) that supports uncontrolled proliferation independent of oxygen availability

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Our results provide a possible mechanism in which upregulation of phosphorylated p53 and p16 maintain the cell cycle arrest of keloid fibroblasts, and FOXO4-DRI selectively induces apoptosis of keloid senescent fibroblasts by prompting p53-pS15 nuclear exclusion

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