Fig. 6
From: Triple negative breast cancer metastasis is hindered by a peptide antagonist of F11R/JAM‑A protein
Effect of F11R/JAM-A-derived peptide (P4D) on the cell monolayer permeability measured by EVOM3 instrument. The cells were untreated (Ctrl), treated with the control scrambled peptide (Scr) or with the F11R/JAM-A antagonistic peptide (P4D) at a concentration of 500 μM. The monolayer permeability is inversely proportional to TEER (trans epithelial/endothelial electrical resistance) values, specified in Ω × cm2. The data were tested for normality by Shapiro–Wilk W test: EA.hy926–failed (P-values for Ctrl: 0.0016, for Scr: 0.0114, for P4D: 0.0875); HMEC-1–passed (P-values for Ctrl: 0.7985, for Scr: 0.5107, for P4D: 0.0630); for MDA-MB-231–passed (P-values for Ctrl: 0.3698, for Scr: 0.0679, for P4D: 0.3424). The permeability results obtained with EA.hy926 cells were analyzed by Kruskal–Wallis test: P = 0.0020–the mean TEER values are significantly different. Dunn’s multiple comparisons test of data obtained on EA.hy926 cells revealed, that permeability of P4D group differs significantly from control groups: Ctrl vs. Scr P > 0.9999; Ctrl vs. P4D P = 0.0084; Scr vs. P4D P = 0.0056. The results of HMEC-1 and MDA-MB-231 monolayer permeability measurements were tested by ordinary one-way ANOVA. For HMEC-1 cells the differences between the groups were statistically significant: P = 0.0067. As evidenced by Tukey’s multiple comparisons test for data derived on HMEC-1 cells, the permeability of P4D group differs significantly from control groups: Ctrl vs. Scr P = 0.9876; Ctrl vs. P4D P = 0.0175; Scr vs. P4D P = 0.0123. For MDA-MB-231 cells the differences between the groups were missing the statistical significance: P = 0.4909