Fig 2: ECD mRNA levels are up-regulated in GC compared to normal gastric mucosa, and silencing of ECD induces G2/M arrest and apoptosis, and inhibits colony formation in GC cells(A, B) SGC-7901 and MGC-803 cells were transfected with the indicated siRNAs, the distribution of cell cycle (A) and apoptosis (B) were measured using flow cytometry. (C) Colony formation abilities between SGC-7901-ECD shRNA cells with stable ECD knockdown and SGC-7901-NC shRNA cells were measured for two weeks. The image and colony numbers of cellular clones with more than 30 cells are shown in the up and down sides (n = 3). (D) SGC-7901 and MGC-803 cells were transfected with the indicated siRNAs, colony formation abilities were detected after two weeks transfection. (E) ECD mRNA levels were up-regulated in the Figure 1C database. (F) ECD mRNA levels were increased in the Figure 1D database. (G) Analysis showing linear regressions and Pearson correlations of ACK1 with ECD in gastric tumor samples in the Figure 1C database (n = 68).

Fig 3: Silencing of ECD blocks the phenotypes generated by ACK1 over-expression(A, B) SGC-7901 cells were transfected with the indicated siRNAs, and the distribution of cell cycle (A) and apoptosis (B) were measured using flow cytometry. (C) SGC-7901 cells were transfected with an ACK1 plasmid together with anti-ECD siRNA, and colony formation abilities were measured for two weeks. The image and colony numbers of cellular clones with more than 30 cells are shown in the left and right sides (n = 3).