Fig. 2

Target cell killing by KIL at low E:T ratios is enhanced following WEE1 kinase inhibition. a Loss of cell index of MOC2 oral carcinoma cells following the addition of KIL at increasing E:T ratios was measured via real-time impedance analysis. Vertical line at 18 h indicates time at which KIL were added. Control cells were exposed to KIL media alone. b % loss of cell index at 12 h after addition of KIL (black line) or sorted WT B6 NK cells (grey line) quantified on left. On right, for comparison, KIL (black line) or sorted WT B6 NK cells (grey line) were used to induce indium release in a standard 12-h radioactive compound release assay. c % loss of cell index at 72 h after addition of KIL (black line) or sorted WT B6 NK cells (grey line) quantified. For B&C, * indicates significantly enhanced killing with KIL cells compared to sorted WT B6 NK cells. d Loss of MOC2 cell index following the addition of KIL at low E:T ratios in the presence of AZD1775 (250 nM) or DMSO (volume equivalent). When AZD1775 was present, MOC2 cells were plated in drug at the start of the assay. Maximum loss of cell index was achieved by addition of triton to some wells. % loss of cell index 48 h after the addition of KIL to MOC2 cells is quantified on right. e % loss of cell index of MOC2 cells in the presence (AZD1775 250 nM) or absence (DMSO volume equivalent) of WEE1 kinase inhibition 12 h after the addition of KIL at the indicated E:T ratios quantified on left. On right, for comparison, the same was measured in a standard 12-h radioactive compound release assay. f % loss of cell index of MOC2 cells 48 h after the addition of KIL. g Impedance analysis of MOC2 cells alone (5 × 10³ cells/well) compared to media or KIL cells alone up to an E:T ratio equivalent of 50:1 (2.5 × 10⁵ KIL/well). Results presented are representative of three independent experiments with similar results. *, p < 0.05; ***, p < 0.001