Fig. 4

CDH11 is responsible for C12orf59-induced GC cell invasiveness and EMT. a The five genes, CDH11, CXCR6, FLT4, PTEN, and TNFSF10, were examined 2-fold mRNA differential expression in MKN-45/shC12orf59 cells compared with that in MKN-45/shControl cells by using a Human Tumor Metastasis RT2 Profiler PCR Array. b Silence of C12orf59 by shRNA in MKN-45 cells substantially downregulated CDH11 and CXCR4 expression as examined by western blotting. c The expression level of C12orf59 and CDH11 were positively correlated in the training cohort of 170 GC samples examined. d Wound-healing assays showed that CDH11 overexpression increased the migratory ability of C12orf59-depleted MKN-45 cells. e Transwell analysis indicated that CDH11 overexpression enhanced the migratory and invasive abilities of C12orf59-depleted MKN-45 cells. f Western blotting shows that after restoration of CDH11 in MKN-45/ shC12orf59 cells, the levels of E-cadherin and α-catenin decreased, whereas the levels of fibronectin and vimentin increased. g IF staining demonstrates a downregulated expression of E-cadherin and an upregulated expression of vimentin in MKN-45/shC12orf59 cells, after overexpression of CDH11. h and i. Restoration of CDH11 antagonized the inhibitory effects of C12orf59 knockdown on the abilities of capillary tube formation (h) and in vitro migration (i) of HUVECs