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. Author manuscript; available in PMC: 2014 Jun 1.
Published in final edited form as: Mol Cancer Ther. 2013 Mar 29;12(6):1099–1111. doi: 10.1158/1535-7163.MCT-12-0737

Figure 4.

Figure 4

SCLIP was involved in pPEA-15-mediated paclitaxel sensitization. In paclitaxel-untreated SKOV3.ip1 stable cells, SCLIP (A) mRNA levels were determined by RT-PCR and (B) protein levels by western blotting (upper panel) and densitometric quantification (lower panel). C, SKOV3.ip1 stable cells were treated with paclitaxel, and 36 hours later, SCLIP expression was determined by western blotting (upper panel) and densitometric quantification (lower panel). β-actin served as a loading control. Vector, SKOV3.ip1-vector; AA, SKOV3.ip1-AA (stably expressing nonphosphorylatable PEA-15 at Ser104 and Ser116, which were substituted with alanine); DD, SKOV3.ip1-DD (stably expressing phosphomimetic PEA-15 at Ser104 and Ser116, which were substituted with aspartic acid). D, OVTOKO cells were treated with SCLIP-targeting siRNA, and SCLIP expression was determined by western blotting 72 hours later (upper panel). β-actin served as a loading control. Following SCLIP silencing, the sensitivity of OVTOKO cells to paclitaxel was determined by trypan blue exclusion assay 72 hours after paclitaxel treatment (lower panel). E, OVCA 432 were transiently transfected with pCMV6-Entry vector or pCMV6-Entry vector carrying SCLIP, and SCLIP expression was determined by western blotting 48 hours later (upper panel). β-actin served as a loading control. Following SCLIP overexpression, the sensitivity of OVCA 432 cells to paclitaxel was determined by trypan blue exclusion assay 72 hours after paclitaxel treatment (lower panel). *, P < 0.05; **, P < 0.01; #, P < 0.001.