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. Author manuscript; available in PMC: 2015 Mar 7.
Published in final edited form as: Cancer Res. 2014 Feb 24;74(8):2258–2269. doi: 10.1158/0008-5472.CAN-13-2459

Figure 4.

Figure 4

Involvement of RSF1-induced NF-κB activation in paclitaxel resistance. A, SKOV3 cells with a Tet-off RSF1 induction system were used. The cells were transiently transfected with a pNF-κB–Luc vector, and luciferase activity was assessed. B, OVCAR3 cells were transiently cotransfected with RSF1 shRNAs and a pNF-κB–Luc vector, and luciferase activity was assessed. Data are representative of three different experiments and are shown as the mean ± SD. *, P < 0.05 compared with the RSF1 no induction group or the control shRNA group. C, OVCAR3 cells were pretreated with the IκBα inhibitor, Bay 11-7082 (0.5 or 1 μmol/L), or the proteasome inhibitor, MG132 (0.062 or 0.125 μmol/L), for 1 hour and then treated with paclitaxel (5 nmol/L). After 48 hours, cytotoxicity was examined using an MTT assay. *, P < 0.05 compared with the group untreated with an inhibitor. #, P < 0.05 compared with the paclitaxel treatment group with no RSF1 induction. D, SKOV3 cells with a Tet-off RSF1 induction system were used. The cells were treated with paclitaxel (5 nmol/L) in the presence or absence of Bay 11-7082 (1 μmol/L) or MG132 (0.125 μmol/L) for 48 hours. Cytotoxicity was examined using an MTT assay. *, P < 0.05 compared with a paclitaxel-treated but inhibitor-untreated group. E, OVCAR3 cells were transfected with specific siRNA (CFLAR, XIAP, BCL2 and BCL2L1, and PTGS2) or control siRNA. After 24 hours, cells were treated with paclitaxel (5 nmol/L). After 48 hours, cytotoxicity was determined using an MTT assay. *, P < 0.05 compared with the control siRNA transfected group. Data are representative of three different experiments and are shown as the mean ± SD.