SOX11 promotes in vitro CXCL12-mediated chemotaxis through CXCR4/FAK signaling activation in MCL. (A-B) 5 × 10⁵ SOX11⁺ MCL cells in in vitro models (Z138CT and JVM2SOX11⁺) and their SOX11⁻ counterparts (Z138KD and JVM2CT MCL cell lines, respectively) untreated (Ø) or pretreated for 6 hours with 10 µM of specific FAK inhibitor (PF) or for 1 hour with 40 µM of the CXCR4 antagonist (AMD) were seeded in the upper chamber of FN-coated transwells (A) or transwells coated with HUVEC cells (B). After overnight incubation, Z138CT- and Z138KD-migrated (left) and JVM2SOX11⁺ and JVM2CT-migrated (right) cells toward recombinant CXCL12 at the bottom chamber of the transwells were quantified by FC. (C) Same CXCL12-mediated chemotaxis assays as in panel A were performed using MCL cells derived from PB (>95% purified) of human primary MCL (5 SOX11⁺ and 4 SOX11⁻ MCL primary cells). (D) 5 × 10⁵ MCL cells from MCL primary tumors (5 SOX11⁺ and 3 SOX11⁻ MCL cases) were seeded on the upper chamber of transwells coated with HUVEC cells. After overnight incubation, migrated cells toward recombinant CXCL12 at the bottom chamber of the transwell were quantified by FC. Migration index was calculated as number of MCL cells that migrated in the presence of the chemoattractant (CXCL12-dependent migration) divided by the number of migrated cells in the absence of the chemokine (unspecific migration). Bar plot represents the mean percentage ± standard deviation of 3 independent experiments. The significance of difference was determined by independent samples Student t test: *P < .05, **P < .01, ***P < .001.