Fig. 4

Olaparib treatment enhances ADCC using both cetuximab and avelumab without modulation of mAb targets EGFR and PD-L1. a Treatment with cetuximab (cet) significantly increased NK-induced lysis of olaparib (ola)-treated BRCA mutant prostate carcinoma (22RV1) cells at 12 h. The addition of anti-CD16 antibody neutralized this increase, confirming that the increased lysis is attributable to ADCC. b STING is not expressed in 22RV1 either before or after olaparib treatment. c Olaparib treatment did not result in significant modulation of EGFR expression on 22RV1 cells as measured by flow cytometry. d Treatment with cetuximab increased NK-induced lysis of olaparib-treated BRCA WT prostate carcinoma cells (DU145) cells. Role of anti-CD16 antibody on increased lysis attributable to ADCC. e The PD-L1+ cell line DU145 also underwent NK-induced ADCC in the presence of the anti-PD-L1 antibody avelumab (ave). Lysis of DU145 cells after 12 h in the presence or absence of olaparib and NK, treated with either avelumab or isotype control is shown. f STING was upregulated in DU145 following exposure to olaparib. g Olaparib treatment did not result in significant modulation of EGFR expression in DU145 cells as measured by flow cytometry. h Olaparib treatment did not result in significant modulation of PD-L1 expression in DU145 cells as measured by flow cytometry. These experiments were performed twice with similar results. p < 0.05*, p < 0.0001****