BTG1 inactivation promotes BCAR1 driven dissemination of lymphoma. (A) Representative western blot and quantification of BCAR1^Y410 phosphorylation in TMD8-BTG1^−/− and TMD8-BTG1^WT cells (representative of n = 4 experiments, P < .05). (B) Western blot analysis of BCAR1^Y410 phosphorylation of sorted splenic B lymphocytes from Btg1^WT or Btg1^−/− mice (n = 2 per group). (C) Immunoprecipitation (representative of n = 3 experiments) and quantification of RAC1-GTP in TMD8-BTG1^−/− and TMD8-BTG1^WT cells (P < .05). (D) Representative confocal images of phalloidin staining and (E) quantification of TMD8-BTG1^WT-BCAR1^−/−, TMD8-BTG1^−/−-BCAR1^WT, and TMD8-BTG1^−/−-BCAR1^−/− cell area on fibronectin-coated slides (P < .0001 compared with TMD8-BTG1^WT-BCAR1^WT). (F) Resistivity measurement estimated by the cell index (Xcelligence) of TMD8-BTG1^−/− cells on fibronectin-coated wells after dasatinib pretreatment (excipient, 0.01 and 0.1 μM for 30 minutes). (G) Flow cytometry quantification of TMD8-BTG1^−/− cells in the spleen and liver of recipient NSG mice treated by 5 daily injections of dasatinib (n = 5) or vehicle (n = 6), (P < .01 compared with vehicle). (H) Kaplan-Meier survival probability of NSG mice after intrasplenic injection of TMD8-BTG1^−/− cells and treatment with vehicle (blue, n = 5) or dasatinib (orange, n = 5; ∗∗P = .0041). Values represent mean ± SEM; ∗P < .05; ∗∗P < .01; ∗∗∗∗P < .0001; using the Mann-Whitney test in panels A,C,G, one-way ANOVA with Dunnett multiple comparisons test in panel E, and log-rank test in panel H. ANOVA, analysis of variance; ns, not significant; SEM, standard error of the mean.