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. 2016 Apr 7;1(4):e86082. doi: 10.1172/jci.insight.86082

Figure 2. Focal adhesion kinase inhibition decreases survival, clonogenicity, and adhesion of BCR-ABL1+ B progenitor acute lymphoblastic leukemia cells in vitro.

Figure 2

(A) Human BCR-ABL1+ (Ph+) IK6+ h9407 B progenitor acute lymphoblastic leukemia (B-ALL) cells and murine Ph+ pre-B cells expressing empty vector (MIG), IK6+, or the IK1 D186A point mutation have decreased viability when treated with VS-4718 at concentrations above 0.1 μM. (B) Decreased numbers of VS-4718–treated h9407 cells are the result of increased apoptosis. (C) The colony-forming potential of single cell-sorted Ph+ murine pre-B cells of the indicated genotypes is greatly reduced in the presence of VS-4718 at a concentration (0.1 μM) that does not affect cell proliferation or viability. (D) Murine pre-B cells of the indicated genotypes are less adherent to RetroNectin monolayers due to focal adhesion kinase (FAK) inhibition after short-term exposure to VS-4718. (E) Reverse-phase protein array (RPPA) analysis of key FAK pathway targets in human Ph+ IK6+ B-ALL (h9407) cells treated with either vehicle or VS-4718 for 24 hours in vitro. Data represent averages ± SD; n = 3 biological replicates each in A and C, 3 technical replicates in B and D, and 4 technical replicates of 2 biologic replicates in E. *P ≤ 0.05, **P ≤ 0.005, ***P ≤ 0.0005, 2-tailed Student’s t test in B–E with 2-way ANOVA in E. MIG, MSCV-IRES-GFP (empty GFP vector).