Figure 5
Figure 5. Targeting the LYN/HS1 axis affects the cytoskeletal functionality and cell viability of a sizable portion of CLL patients. (A) In the dot plot, chemotaxis toward CXCL12 was evaluated in 19 CLL primary samples after treatment with 100 nM dasatinib. CLL cases are divided based on LYN/HS1 activation status in active-HS1 (n = 11) and inactive-HS1 (n = 8). Means ± SEM of the migration indexes after treatment (as a percentage of the untreated control; see “Materials and methods”) are displayed, and significant chemotaxis reduction of active-HS1 cells was observed, as compared with inactive-HS1 cells. (B) In the dot plot, CXCL12-induced F-actin polymerization was evaluated in 18 CLL primary samples after treatment with 100 nM dasatinib. CLL cases were divided based on LYN/HS1 activation status in active-HS1 (n = 8) and inactive-HS1 (n = 10). Means ± SEM of the F-actin polymerization after treatment (as a percentage of the untreated control; see “Materials and methods”) are displayed, and significant F-actin polymerization reduction of active-HS1 cells was observed as compared with inactive-HS1 cells. (C) In the dot plot, spontaneous adhesion to BSA-coated plates was evaluated in 16 CLL primary samples after treatment with 100 nM dasatinib. CLL cases are divided based on LYN/HS1 activation status in active-HS1 (n = 8) and inactive-HS1 (n = 8). Means ± SEM of the spontaneous adhesion after treatment (as a percentage of the untreated control; see “Materials and methods”) are displayed, and significant spontaneous adhesion reduction of active-HS1 cells was observed, as compared with inactive-HS1 cells. (D) In the dot plot, adhesion to HS5 stroma was evaluated in 16 CLL primary samples after treatment with 100 nM dasatinib. CLL cases are divided based on LYN/HS1 activation status in active-HS1 (n = 8) and inactive-HS1 (n = 8). Means ± SEM of the adhesion to HS5 after treatment (as a percentage of the untreated control; see “Materials and methods”) are displayed, and significant reduction of active-HS1 cell adhesion to HS5 was observed, as compared with inactive-HS1 cells. (E) In the dot plot, viability after 48 hours of 100 nM dasatinib treatment was evaluated in 32 primary CLL samples, divided based on LYN/HS1 activation status in active-HS1 (n = 18) and inactive-HS1 (n = 14). Means ± SEM of the viability after treatment (as a percentage of the untreated control) assessed by luminescence-based detection of cellular adenosine triphosphate content are displayed, and preferential viability reduction of active-HS1 cells was observed. **P ≤ .01; ***P ≤ .001, not significant, Mann-Whitney U test.

Targeting the LYN/HS1 axis affects the cytoskeletal functionality and cell viability of a sizable portion of CLL patients. (A) In the dot plot, chemotaxis toward CXCL12 was evaluated in 19 CLL primary samples after treatment with 100 nM dasatinib. CLL cases are divided based on LYN/HS1 activation status in active-HS1 (n = 11) and inactive-HS1 (n = 8). Means ± SEM of the migration indexes after treatment (as a percentage of the untreated control; see “Materials and methods”) are displayed, and significant chemotaxis reduction of active-HS1 cells was observed, as compared with inactive-HS1 cells. (B) In the dot plot, CXCL12-induced F-actin polymerization was evaluated in 18 CLL primary samples after treatment with 100 nM dasatinib. CLL cases were divided based on LYN/HS1 activation status in active-HS1 (n = 8) and inactive-HS1 (n = 10). Means ± SEM of the F-actin polymerization after treatment (as a percentage of the untreated control; see “Materials and methods”) are displayed, and significant F-actin polymerization reduction of active-HS1 cells was observed as compared with inactive-HS1 cells. (C) In the dot plot, spontaneous adhesion to BSA-coated plates was evaluated in 16 CLL primary samples after treatment with 100 nM dasatinib. CLL cases are divided based on LYN/HS1 activation status in active-HS1 (n = 8) and inactive-HS1 (n = 8). Means ± SEM of the spontaneous adhesion after treatment (as a percentage of the untreated control; see “Materials and methods”) are displayed, and significant spontaneous adhesion reduction of active-HS1 cells was observed, as compared with inactive-HS1 cells. (D) In the dot plot, adhesion to HS5 stroma was evaluated in 16 CLL primary samples after treatment with 100 nM dasatinib. CLL cases are divided based on LYN/HS1 activation status in active-HS1 (n = 8) and inactive-HS1 (n = 8). Means ± SEM of the adhesion to HS5 after treatment (as a percentage of the untreated control; see “Materials and methods”) are displayed, and significant reduction of active-HS1 cell adhesion to HS5 was observed, as compared with inactive-HS1 cells. (E) In the dot plot, viability after 48 hours of 100 nM dasatinib treatment was evaluated in 32 primary CLL samples, divided based on LYN/HS1 activation status in active-HS1 (n = 18) and inactive-HS1 (n = 14). Means ± SEM of the viability after treatment (as a percentage of the untreated control) assessed by luminescence-based detection of cellular adenosine triphosphate content are displayed, and preferential viability reduction of active-HS1 cells was observed. **P ≤ .01; ***P ≤ .001, not significant, Mann-Whitney U test.

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