FDX1 and hepatocellular carcinoma: Crucially, FDX1-knockdown (si-FDX1) and pharmacological inhibition experiments using the copper chelator tetrathiomolybdate (TTM) were performed to establish causality and pathway specificity.<h4>Result</h4>Emodin treatment dose-dependently inhibited HCC cell proliferation, promoted apoptosis, elevated intracellular copper levels, and reduced GSH.