Figure 1

Panel A PLX4720 inhibit the basal CXCL8 secretion in BCPAP (ANOVA F: 14.3; p < 0.0001), the inhibitory effect was significant starting by 2 µM concentration (Post Hoc analysis by Bonferroni *p < 0.001 vs. basal). Panel B PLX4720 inhibited the basal CXCL8 secretion in 8305C (ANOVA F: 407.9; p < 0.0001) (ANOVA F: 407.9; p < 0.0001), the inhibitory effect was significant starting from 0.1 µM (Post Hoc analysis by Bonferroni *p < 0.001 vs. basal, **p < 0.001 vs. 0,1 µM). Panel C PLX4720 inhibited the basal CXCL8 secretion in 8505C (ANOVA F: 55.24; p < 0.0001), the inhibitory effect started from 0.1 µM (Post Hoc analysis by Bonferroni *p < 0.001 vs. basal, p < 0.001 vs. 0.1 µM). Panel D Basal secretion of CXCL8 was not inhibited by PLX4720 in TPC-1 cell lines at any concentrations (ANOVA F: 1.8, p = 1.34). Panel E Basal secretion of CXCL8 was inhibited by PLX4720 in NHT (ANOVA F: 13.13; p < 0.001) being significant only at the higher concentration of 10 µM (Post Hoc analysis by Bonferroni *p < 0.01 vs. basal). Panel F PLX4720 inhibit the TNF-𝛼-stimulated CXCL8 secretion in BCPAP (ANOVA F: 12.29 p < 0.0001), the inhibitory effect was significant starting by 1 10 µM (3.13; t anPost Hoc analysis by Bonferroni *p < 0.001 vs. TNF-𝛼). Panel G PLX4720 inhibit the TNF-α-stimulated CXCL8 secretion in 8305C (ANOVA F: 5.76 p < 0.0001), the inhibitory effect started from 1 rom Post Hoc analysis by Bonferroni *p < 0.001 vs. TNF-𝛼). Panel H PLX4720 inhibit the TNF-𝛼-stimulated CXCL8 secretion in 8505C (ANOVA F: 42.85 p < 0.0001), the inhibitory effect started from 0.1 rom Post Hoc analysis by Bonferroni *p < 0.001 vs. TNF-𝛼, **p < 0.001 vs. 0.1 ni *p < Panel I TNF-𝛼-stimulated CXCL8 secretion was not inhibited by PLX4720 in TPC-1 cell lines at any concentrations (ANOVA F: 1.6, p = 1.78). Panel E TNF-𝛼-stimulated CXCL8 secretion was inhibited by PLX4720 in NHT (ANOVA F: 2.5; p < 0.01) being significant only at the higher concentration of10 µM (Post Hoc analysis by Bonferroni *p < 0.001 vs. TNF-α alone).