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The investigated effects could be reversed using a neutralizing anti-CD74 antibody, and Cd74 mice developed fewer tumours associated with decreased proliferation rates. We identified a pro-tumorigenic role of MIF during proliferation and therapy-induced apoptosis of HCC cells. These effects were mediated via the MIF cognate receptor CD74. Thus, inhibition of the MIF/CD74 axis could represent a promising target with regard to new pharmacological therapies aimed at HCC. We identified a pro-tumorigenic role of MIF during proliferation and the
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