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Potential Cancer Drug Mobilizes Immunity by Suppressing SUMOylation

A new study shows TAK-981, a potent and selective inhibitor of SUMOylation, induces IFN1 signaling and protects the IFN1 pathway from inactivation within tumors. The inhibitor activates T cells and dendritic cells that present antigens to the adaptive immune system, in both mouse models and in cell lines. The activity of the potential cancer drug depends on the IFN1 pathway and adaptive immunity to suppress tumor growth. Combined with anti-PD1 antibody TAK-981 demonstrates prolonged survival in tumor-bearing mice and increased activation of natural killer cells and CD8 expressing T cells.