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Fig. 3 | Molecular Cancer

Fig. 3

From: STK3 promotes gastric carcinogenesis by activating Ras-MAPK mediated cell cycle progression and serves as an independent prognostic biomarker

Fig. 3

STK3 promotes tumorigenesis by activating the Ras-MAPK pathway and serves as an independent prognostic biomarker. a, b STK3 was highly expressed in cancer cells, endothelial cells, and cancer associated fibroblasts. c The t-SNE plots of high and low expression populations of STK3, CDK4, and CCND2 in GC single-cell resolution. d The activities of cell cycle regulation, Ras signaling pathway, MAPK signaling pathway in GC cells. e In single-cell level, DEGs (in rows, q-value < 10− 10) between STK3 high and low expression were enriched in cell proliferation-related pathway by GO enrichment analysis. f Regulation of mitotic cell cycle was positively correlated with high expression of STK3 through GSEA from single-cell resolution (P < 0.001). g The proliferation and apoptosis biomarkers along with the functional pseudotime in GC development. STK3 was co-upregulated with proliferation biomarkers in the early state of tumor development. h Representative images of IHC staining of STK3 from GC tissue microarray. STK3 was predominantly localized in the cytoplasm of the cancer cells, while it demonstrated negative expression in the adjacent epithelium tissue. i STK3 was highly expressed in both intestinal-type and diffuse-type GC samples. j, k Overexpressed STK3 was associated with poor disease-specific survival in primary GCs (TCGA cohort, n = 375, P = 0.035; Hong Kong cohort, n = 263, P < 0.001). l, m STK3 abundance predicted poor disease-specific survival in intestinal-type GC patients (TCGA cohort, n = 164, P = 0.162; Hong Kong cohort, n = 141, P < 0.001). n, o In diffuse-type GCs, the upregulation of STK3 was associated with unfavorable clinical outcomes (TCGA cohort, n = 73, P = 0.331; Hong Kong cohort, n = 122, P < 0.001)

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