Fig. 7

c-MYC and its target genes are regulated by IFITM3 in GC oncogenesis and chemoresistance. A Gene Set Enrichment Analysis (GSEA) was carried out to analyze the co-expression network and determine Pearson’s correlation coefficient between IFITM3 and other hallmarks of cancer in cBioPortal. The right panel represents an enrichment plot of IFITM3-correlated genes in c-MYC-regulated targets. B Spearman rank correlation coefficient of individual genes (including PSMA1, PSMA6, PSMB2, HDAC2, LDHA and SPRING) against IFITM3 in 71 GC tissues from Cho Gastric dataset (GSE138861). C Quantitative RT-PCR analyses were conducted on the six c-MYC target genes for their gene expression in TMK-1 IFITM3-overexpression or TSGH IFITM3-depletion models (*p < 0.05, **p < 0.01). D Western blot analyses of IFITM3 and c-MYC expression in control or IFITM3-overexpressing TMK-1 cells with or without c-MYC knockdown. Cellular growth curves (E) and migration rates (F) of the same experimental groups were determined by measuring viable and migrated cell numbers, respectively. G Sphere formation assays were performed to assess the influences c-MYC knockdown on IFITM3-overexpressing TMK-1 cells. (Left panel, scale bar, 500 μm; right panel is the statistical results, **p < 0.01) H Chemosensitivities of the same indicated groups of TMK-1 cells were determined based on the relative number of cells survived after treatment with 5’FU (20 μg/ml) or cisplatin (3 μM) for 72 h. *p < 0.05, **p < 0.01.