Fig 1: JAML promoted GC cell proliferation and migration. (A) The expression of JAML in GC cell lines (AGS, HGC-27, MKN-28). (B) Quantitative analysis of (A) n=3, unpaired t test, *P < 0.05, compared with AGS group. (C) Knockdown efficiency of JAML was confirmed in MKN-28 cells after transient transfection of SiRNA for 72h by western blot. (D) Quantitative analysis of (C) n=3, unpaired t test, **P < 0.01, compared with siNC group; n=3, unpaired t test, *P < 0.05, compared with siNC group; n=3, unpaired t test, ns, P>0.05, compared with siNC group. (E) Knockdown efficiency of JAML in MKN-28 cells after transient transfection of siRNA for 120h by western blot. (F) Quantitative analysis of (E) n=3, unpaired t test, *P < 0.05, compared with siNC group. (G) Wound healing assay was performed in transfected MKN-28 cells treated with or without siRNA to evaluate cell migration. (H) Transwell migration assay to assess cell migration. (I) EdU incorporation assay to observe cell proliferation. (J) Quantitative analysis of (G) n=3, unpaired t test, **P < 0.01, compared with siNC group. (K) Quantitative analysis of (H) n=15, unpaired t test, ****P < 0.0001, compared with siNC group. (L) Quantitative analysis of (I) n=9, unpaired t test, **P < 0.01, compared with siNC group. siNC, negative control.
Fig 2: (A) JAML expression in HGC-27 cells after transfection with JAML plasmid for 72h. (B) Quantitative analysis of (A) n=3, unpaired t test, **P < 0.01, compared with NC group. (C) JAML expression in HGC-27 cells after transfection with JAML plasmid for 120h. (D) Quantitative analysis of (C) n=3, unpaired t test, *P < 0.05, compared with NC group. (E) Wound healing assay to assess cell migration in HGC-27 cells. (F) Quantitative analysis of (E) n=3, unpaired t test, ***P < 0.001, compared with NC group. (G) Transwell migration assay to evaluated cell migration in HGC-27 cells. (H) Quantitative analysis of (G) n=9, unpaired t test, **P < 0.01, compared with NC group. (I) EdU incorporation assay to observe cell proliferation in HGC-27 cells. (J) Quantitative analysis of (I) n=6, unpaired t test, *P < 0.05, compared with NC group. NC, negative control.
Fig 3: Expression of JAML in human gastric cancer (GC) and peritumoral tissues. (A) JAML expression on cytoplasm and membrane of GC cells. (B) The JAML expression in GC and peritumoral tissues. (C) Quantitative analysis of JAML expression in GC and peritumoral tissues. n=63, paired t test, ****P < 0.0001, compared with peritumoral tissues.
Fig 4: JAML promoted GC cell migration and proliferation by activating p38 signaling pathway. (A) The effect of JAML silencing on the phosphorylation of p38, ERK and JNK. (B–D) Quantitative analysis of (A) n=3, unpaired t test, *P < 0.05, compared with siNC group; ns, P > 0.05, compared with siNC group. (E) The effect of SB-203580 on p38 phosphorylation. (F) Quantitative analysis of (E) n=3, unpaired t test, **P < 0.01, compared with DMSO group. (G) Transwell migration assay to evaluate the effect of SB-203580 on cell migration in MKN-28 cells. (H) Quantitative analysis of (G) n=9, unpaired t test, ***P < 0.001, compared with DMSO group. (I) EdU incorporation assay to assess the effect of SB-203580 on cell proliferation in MKN-28 cells. (J) Quantitative analysis of (I) n=9, unpaired t test, ****P < 0.0001, compared with DMSO group.
Supplier Page from Abcam for Anti-JAML antibody [EPR15289]