Non-transmissible Sendai virus vector encoding c-myc suppressor FBP-interacting repressor for cancer therapy

Figure 6 SAP155 siRNA induces c-Myc activation with ErK phosphorylation, but suppresses phosphorylated-cdk2/cyclinE expression. HeLa cells were treated with SAP155 siRNA for three days (72 h). A: SAP155 siRNA, as well as SSA treatment, increased not only c-Myc expression level, but also c-Myc phosphorylation at both Ser62, but suppressed phosphorylated-cdk2 and cyclinE in a dose-dependent manner. Thus, SAP155 siRNA activates c-Myc potentially via inhibiting endogenous FIR pre-mRNA splicing; B: FIR Sendai virus (SeV/dF/FIR) reversed the cytotoxicity of SSA by suppressing activated endogenous c-Myc. HeLa cells were treated with 50 ng/mL SSA for 48 h with control (MetOH and H₂O). 10 MOI of SeV/dF/FIR apparently suppressed activated c-Myc expression, whereas SeV/dF/FIR did not influence basal expression (MetOH or H₂O). FIR: FBP Interacting Repressor; FBP: FUSE-Binding protein; FUSE: Far Upstream Element; SeV: Sendai virus; GFP: Green fluorescent protein; MOI: Multiplicity of infection; SSA: Spliceostatin.