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. Author manuscript; available in PMC: 2014 Feb 5.
Published in final edited form as: Cancer Gene Ther. 2011 Jun 24;18(8):598–608. doi: 10.1038/cgt.2011.30

Figure 5.

Figure 5

Susceptibility of gemcitabine-resistant pancreatic adenocarcinoma cells to measles virus (MV) infection and cytotoxic efficacy of activated fludarabine. (a) Naive or gemcitabine-resistant pancreatic adenocarcinoma cells were infected with MV-enhanced green fluorescent protein (EGFP) or MV-EGFP-anti-PSCA at a multiplicity of infection (MOI) of 1 and syncytia formation was analyzed 72 h post-infection (p.i.) (means of 3 wells per cell line). Differential viral permissiveness is expressed as the ratio between numbers of syncytia per well induced by the virus variants with unmodified H vs retargeted anti-PSCA (left y axis, white bars) and sizes of the respective syncytia are indicated as nuclei per syncytium (right y axis; black triangle: MV-EGFP; white triangle, MV-EGFP-anti-PSCA). (b) Cytotoxic efficacy of activated fludarabine. Different fractions (0.01, 0.1 and 0.5) of conditioned media (identical preparation procedure as described in legend to Figure 3) were added to a fresh layer of test cells. Cell viability was determined after 72 h by XTT (2,3-bis-(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide) assay. Means and standard deviations of samples normalized to mock-treated cells from three experiments are shown (light gray bars, naive cells; light gray-shaded bars, gemcitabine-resistant cells).