Fig. 3: VSV∆51-amiR-4 infection and inhibition of EZH2 via GSK126 promote synthetically lethal conditions and potentiate anti-tumour therapy. | Nature Communications

Fig. 3: VSV∆51-amiR-4 infection and inhibition of EZH2 via GSK126 promote synthetically lethal conditions and potentiate anti-tumour therapy.

From: Virally programmed extracellular vesicles sensitize cancer cells to oncolytic virus and small molecule therapy

Fig. 3

a, b When exposed to low viral doses of VSV∆51-amiR-4 and 2–3 doses of GSK126 (15 μM) depending on the cell line, cell death is increased in a panel of cancer cell lines (HPAF-II, BxPC-3, 786-0) and a primary patient-derived pancreatic cancer cell line (P025), as assessed by representative crystal violet staining images of four biological replicates (a) and corresponding cell viability quantification compared to mock-infected DMSO-treated cells (b); timeline of treatment procedures can be found in Supplementary Fig. 3a. Two-way ANOVA with Sidak’s multiple comparisons test (95% CI), ****P < 0.0001. Shown are the mean values ± SEM of biological triplicates (P025) or quadruplicates (HPAF-II, BxPC-3 and 786-0). c Phase-contrast images (scale bar = 400 μm) and (d) acini diameter fold change compared to the diameter at day 0 of uninfected or VSV∆51-amiR-NTC or VSV∆51-amiR-4-infected BxPC-3 spheroids with or without 15 μM GSK126 treatment. Results displayed as mean ± SEM, n = 3 biological replicates per condition. For day 5, two-way ANOVA with Dunnett’s multiple comparisons test (95% CI), ****P < 0.0001. Source data are provided as a Source data file.

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