Fig. 2
MXRA8 promotes the therapeutic efficacy of OVM in vitro and in vivo. a The infection rates of OVM-GFP in control, ΔMXRA8 (sgRNA-1) and ΔMXRA8 (sgRNA-1)+MXRA8 Hs578T or HepG2 cells (MOI of 0.1 for 48 h at 37 °C) by flow cytometry (three experiments, n = 9; one-way ANOVA; mean ± s.d.). b, c MXRA8-overexpressing cells and control cells were infected with OVM-GFP virus at a multiplicity of infection (MOI) of 1 (HeLa cells, 48 h; HT29 cells, 24 h), after which the phase-contrast and fluorescence microscopy images were captured, and further processed for detection of GFP expression by flow cytometry (three experiments, n = 9; one-way ANOVA; mean ± s.d.). Scale bars: 50 μm. d The viral titer of tumor cells that treated with OVM at 0.01 MOIs for 72 h by CCID50 assay (three experiments, n = 9; one-way ANOVA; mean ± s.d.). e The viability of tumor cells treated with OVM at the respective MOIs for 72 h by MTT assay (three experiments, n = 9; one-way ANOVA; mean ± s.d.). f Timeline of the experimental arrangement for g–o. g Tumor growth curves of the average HT29 tumor volumes in each group. h Kaplan–Meier survival curves of HT29 tumor-bearing mice by log-rank test. i The amount of OVM in tumor tissues was measured by qPCR at 2 days after the 10th injection (n = 4, per group). j Tumor growth curves of the average HeLa tumor volumes in each group. k HeLa tumor weights on the 27th day after the first OVM treatment (one-way ANOVA; mean ± s.d.). l Photograph of HeLa tumor tissues on the 27th day. m Tumor growth curves of the average HepG2 tumor volumes in each group. n HepG2 tumor weights on the 23rd day after the first OVM treatment (one-way ANOVA; mean ± s.d.). o Photograph of HepG2 tumor tissues on the 23rd day. n.d., not detectable. Tumor growth curves were analyzed by repeated-measures ANOVA in a general linear model. *P < 0.05; **P < 0.01; ***P < 0.001
