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Fig. 2 | Journal for ImmunoTherapy of Cancer

Fig. 2

From: Enhanced susceptibility of cancer cells to oncolytic rhabdo-virotherapy by expression of Nodamura virus protein B2 as a suppressor of RNA interference

Fig. 2

VSV∆51-B2 alters cytotoxicity and viral genome cleavage. a Relative metabolic activity of 38 human cancer cell lines infected with VSVΔ51-GFP or VSVΔ51-B2 or additionally VSVΔ51-VP55 for 48 h at an MOI of 1. The results are expressed as a percentage of the signal obtained compared to mock treatment. b Time-course of viral titers from 786-O and M14 cell lines infected with VSVΔ51-GFP or VSVΔ51-B2 at an MOI of 3. NS: P > 0.1, *P < 0.1, **P < 0.01, ***P < 0.001, using Student’s t-test. Only significantly different pairs are indicated on the fig. c We performed small-RNA deep-sequencing using M14 or 786-O cells infected with VSVΔ51-B2 at an MOI of 0.1 for 18 h. B2 expression in VSVΔ51 virus abrogates genomic cleavage as 22-mer vsRNAs are no longer prominent. VSVΔ51-B2 derived vsRNAs display a bias towards positive strand reads in M14 and 786-O cells. d The indicated human cancer cell lines were infected with VSVΔ51-GFP or VSVΔ51-B2 (MOI = 0.1). At the indicated time points, the expression level of virus genomes for each sample was quantified and normalized to GAPDH. Levels of VSV genomes are expressed relative to the level observed in the VSVΔ51-GFP 1 h-post-infection samples, which were arbitrarily set to 1. Error bars indicate ±SD among triplicates. NS: P > 0.1, *P < 0.1, **P < 0.01, ***P < 0.001, using Student’s t-test

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