Fig. 1

STK3 is upregulated in GC patients (***, P < 0.001). a The STK3 genetic alterations (gene amplification, deep deletion, or somatic mutation) and mRNA expression in primary GC samples from the TCGA cohort (total alteration rate: 24%). b The positive correlation of STK3 copy-number alterations with its mRNA expression. c, d STK3 mRNA expression is upregulated in the tumor tissues compared with it in normal tissue group from TCGA and ACRG cohorts. e STK3 is upregulated in tumor samples compared with paired adjacent nontumorous samples. f The STK3 mRNA is differently expressed across five molecular subtypes in TCGA cohort. STK3 was significantly upregulated in EBV-positive and microsatellite-instable types of GC (P < 0.001). g STK3 mRNA expression is abundantly expressed in intestinal-type GCs compared with diffuse-type GCs. h The STK3 mRNA expression in four molecular subtypes proposed by ACRG cohort (P < 0.001). i The STK3 protein expression is increased in GC samples compared with the paired normal controls. j The expression of STK3 is positively correlated with cell cycle genes from TCGA cohort. k The cell cycle-related pathways are positively correlated with high STK3 expression by GSEA (P < 0.05). l STK3-related DEGs (|Fold Change| > 2, P < 0.05) were enriched in cell cycle and DNA replication through KEGG enrichment analysis (FDR < 0.001). m STK3-related DEGs were enriched in cell cycle progression through GO enrichment analysis (FDR < 0.001)