Tuvusertib upregulates the death receptor TRAIL-R2, immune checkpoint ligand PD-L1, and NKG2D ligand ULBP-1 in DU145 cells Gene expression analysis of tuvusertib-exposed DU145 and 22RV1 cells showed a trend toward increased expression of immune checkpoint ligands, increased antigen processing machinery, and decreased expression of immunosuppressive factors (Fig. 2 A,B).
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The ATR inhibitor tuvusertib (M1774) sensitizes prostate carcinoma to natural killer cell-mediated cytotoxicity, which is further augmented by the IL-15 receptor superagonist N-803.
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