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In this study, we systematically demonstrated that both genetic amplification (exogenous overexpression) and pharmacological induction (endogenous upregulation) of ChaC1 profoundly sensitized hepatocellular carcinoma (HCC) cells to auranofin (AUR) cytotoxicity

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Meanwhile, the upregulation of MDM2 suggests that the p53 signaling pathway may be inhibited, which to a certain extent reduces the ability of cells to repair DNA damage and may prompt cells to evade apoptotic mechanisms, further accelerating tumor progression