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. 2018 Feb 26;128(4):1384–1396. doi: 10.1172/JCI97611

Figure 3. Loss of E-cad expression sensitizes tumor cells to NK-mediated cytotoxicity through KLRG1.

Figure 3

(A) A549 cells were transfected with 10 nM of scrambled (SCR) or 3 different E-cad–specific siRNA molecules. After 24 hours, cells were treated with (EMT) or without (NON-EMT) TGF-β (5 ng/ml) for 72 hours. E-cad and GAPDH expressions were assessed by Western immunoblotting. (B) Susceptibility to NK cytotoxicity was assessed using NK92mi cells as effectors, as described for Figure 1. Mean ± SEM is shown; 1-way ANOVA with Tukey’s post hoc analysis was performed, **P < 0.01, ****P < 0.0001. (C) NK92mi cells were transfected with 10 nM of SCR or KLRG1-specific siRNA. After 72 hours, KLRG1 expression was assessed by flow cytometry. gMFI, geometric mean fluorescence intensity. (D) NK92mi cells from C were used as effectors against EMT or non-EMT A549 cells in the NK cytotoxicity assay. Mean ± SEM is shown; 2-way ANOVA with Tukey’s post hoc analysis was performed, **P < 0.01, ****P < 0.0001. All experiments were repeated twice, and data are representative of 1 experiment.