Figure 5.

CAN-induced proliferation inhibition in QBC939 cells involves the activation of the NF-κB pathway. (A) p-IKKα levels in QBC939 cells were elevated following treatment with CAN, in a dose-dependent manner, compared with the control (0 µM). (B) p-IκBα and IκBα levels in cells were significantly increased and decreased, respectively, compared with the control, following treatment with CAN. (C) p-p65 levels in the nucleus were increased by treatment with CAN. (D) CAN increased p-p65 levels, although it had a weak impact on the total p65 protein expression. (E) The dual-luciferase reporter gene assay indicated that CAN may stimulate NF-κB(p65) transcriptional activity. (F) CAPE (1 µM), a specific inhibitor of p65, reduced the CAN-induced nuclear translocation of p-p65 and (G) partially decreased the cytotoxicity of CAN. Data are expressed as the mean ± standard deviation. *P<0.05, **P<0.01 vs. control; ^#P<0.05, CAN+CAPE vs. CAN. CAN, cantharidin; CAPE, caffeic acid phenethyl ester; NF-κB, nuclear factor-κB; IKK, inhibitor of NF-κB kinase; LUC, luciferase; p, phosphorylated; IκBα, NF-κB inhibitor α; Ruc, Renilla luciferase.