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Nevertheless, the aberrant activation of c-Met and downstream signaling pathways through overexpression of HGF or c-Met, gene amplification, mutational activation of c-Met, down-regulation of Met-targeted miRNA, binding to other ligands, autocrine signaling or abnormally high HGF levels initiates and drives tumorigenesis and promotes tumor growth, invasion, metastasis, and angiogenesis in HCC

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This approach enhances treatment efficacy, overcomes resistance, and reduces required doses, minimizing side effects

p53 Suppresses Metabolic Stress-Induced Ferroptosis in Cancer Cells