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Moreover, restored expression of MT1M in the hepatocellular carcinoma cell line, Hep3B, which lacks endogenous MT1M expression, suppressed cell growth in vitro and in vivo and augmented apoptosis induced by tumor necrosis factor [104]

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Subsequent experiments also proved that the TLR3/TIR domain-containing adapter-inducing interferon-β/RIP3 pathway, which is dependent on p53, phosphorylates MLKL and initiates necroptosis [16]