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Figure S2. Suppression or overexpression of C12orf59 did not alter the GC cellular growth rate. (DOCX 155 kb)

Figure S1. TCGA data analysis of C12orf59 expression pattern and prognostic value in GC tissues. a. Expression of C12orf59 mRNA level in 68 paired GC and adjacent normal tissues from TCGA database. The mean level of C12orf59 expression in the GC tissues was significantly higher than in normal tissues (*P

Figure S3. The microvessel density (MVD), as indicated by CD31 staining was noticeably stronger in GC samples with C12orf59 high expression compared with GC samples with C12orf59 low expression in the training cohort of 170 samples. *P

Table S1. List of genes differentially expressed in MKN-45 cells after C12orf59 knockdown using a Human Tumor Metastasis Real-time PCR Array. (DOCX 24 kb)

Figure S4. Restoration of CDH11 in GC cells enhanced the in vivo metastasis ability. Representative hematoxylin and eosin (H&E) staining depicting metastatic tumors in the lung of nude mice that originated from MKN-45/shC12orf59/CDH11 and MKN-45/shC12orf59/control cells injected via the tail vein (left). Number of metastatic nodules formed in the lung of mice 6 weeks after tail vein injection of MKN-45/shC12orf59/CDH11 or MKN-45/shC12orf59/control cells. Six mice per group; **P

Figure S6. miR-654-5p inhibited GC cell invasion and metastatic ability in vitro. a. Overexpression of miR-654-5p dramatically reduced the migratory ability of GC cells in the wound-healing assay. b. Overexpression of miR-654-5p resulted in a decrease in the migratory and invasive abilities of GC cells as determined by Transwell analysis. *P

The clinicopathologic characteristics of the 112 GC patients who received surgery followed by adjuvant chemotherapy in this study. (DOC 40 kb)