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. 2017 Dec 1;20(1):69–79. doi: 10.1016/j.neo.2017.11.003

Figure 7.

Figure 7

Rapamycin combined with cisplatin exerts an anti-UEC effect by IL-27–mediated NK cell's activation. (A, B) After co-culture with rapamycin (100 nM) and/or cisplatin (10 μM)-pretreated Ishikawa cells, the expression of KIR2DL1, KIR3DL1, NKG2D, CD16, NKp46, Granzyme B, and perforin in NK cells (n = 6) was analyzed by FCM. (C) NK cells (n = 6) were treated as described Figure 7A and then co-cultured with fresh Ishikawa cells for the cytotoxicity assay at different E/T ratios (1:100, 1:10, 1:1, 3:1, or 10:1) for 3 hours. (D-I) Ishikawa-xenografted nude mice were intraperitoneally injected with rapamycin (2 mg/kg) and/or cisplatin (2 mg/kg) or PBS for 3 weeks. PKH67-labeled human peripheral NK cells were then adoptively transferred to these Ishikawa-xenografted nude mice (n = 8 mice/group) every 7 days for the first 2 weeks. After 3 weeks, the tumors were obtained for FCM (E, F) to analyze the expression of GP130, WSX-1, NKG2D, CD16, Granzyme B, and perforin in PKH-67–labeled NK cells, and IHC (G) to evaluate the expression of PCNA in cancer lesions. (H) In addition, the tumor volume was measured every other day. (I) Kaplan-Meier survival curves of these Ishikawa-xenografted nude mice. Data are expressed as mean ± SEM. *P < .05, **P < .01, **P < .01, ***P < .001, and ****P < .0001.