Fig 1: OAS1 impacted CTL function and contributed to increased resistance to immunotherapy. The high expression of OAS1 diminishes or even reverses the benefits of CTL infiltration levels on patient survival in LIHC (p = 0.020), COAD (p = 0.022), UCEC (p < 0.001), BLCA (p = 0.035), BRCA (p = 0.024), and LUAD (p = 0.034) (A). In multiple tumors, overexpression of OAS1 corresponds with overexpression of immune checkpoint markers, such as LAG3, CTLA4, PDCD1 (PD-1), IDO1, and CD274 (PD-L1) (B). OAS1 expression coincided with EPCAM at the single-cell level in PAAD (C). Overexpression of OAS1 is linked to the activation of the interferon α (NES = -2.4, FDR <0.001) (D) and γ signaling pathways (NES = -2.4, FDR <0.001) (D, E), as well as the IL6-JAK-STAT3 signaling pathway (NES =-1.98, FDR = 0.01) (D, F). Infection by certain pathogens significantly increases OAS1 expression (H). (*p<0.05, **p<0.01, ***p<0.001).
Fig 2: The prognostic value of OAS1 expression. The OAS1 expression was associated with the prognosis of several tumor types (A). The higher OAS1 expression were linked to shorter OS in LUAD (HR=1.32, p=0.008), LAML (HR=1.43, p=0.05), PAAD (HR=1.66, p=0.047), LGG (HR=1.76, p<0.001), ACC (HR=1.79, p=0.007) (B-F). The higher OAS1 expression were linked to longer OS in MESO (HR=0.91, p = 0.018), SKCM (HR=0.93, p < 0.001), BLCA (HR=0.88, p = 0.009) (G-I). (*p<0.05).
Fig 3: Correlations between OAS1 expression and tumor immune microenvironment. A significant positive correlation between OAS1 expression and macrophage infiltration was observed using the xCell algorithm (A). OAS1 expression and M2 subtype macrophage infiltration was analyzed by the CIBERSORT (B) and QUANTISEQ (C) algorithms. There was positive correlation between OAS1 expression and CD163 in PAAD (R=0.66, p < 0.001) (D), LIHC (R=0.54, p < 0.001) (E), HNSC (R=0.41, p < 0.001) (F), and BRCA (R=0.61, p < 0.001) (G).
Fig 4: The expression of OAS1 in different cancers. The differences in OAS1 expression levels among various normal tissues can be found in the GTEx database(A).The expression of OAS1 was significantly overexpressed in BLCA, BRCA, CESC, CHOL, COAD, ESCA, GBM, HNSC, KIRC, KIRP, LUAD, PCPG, THCA, and UCEC in TCGA database (B). The OAS1 protein was significantly overexpressed in Clear cell RCC, HNSC, UCEC, and PAAD in the CPTAC database (C). There was a correlation between OAS1 expression and the pathological stage of the tumor in BLCA, PAAD, LUAD, and SKCM (D). The boxplot illustrates the differential expression of OAS1 between pancreatic cancer tissues and adjacent non-cancerous tissues in the GSE28735 dataset (E). The OAS1 protein was significantly overexpressed in PAAD using immunohistochemistry data from the XJTU cohort (F, G). (*p<0.05, **p<0.01, ***p<0.001).
Fig 5: The role of OAS1 in PAAD. The PPI network plots showed that differential gene interactions were associated with epithelial differentiation (A). The significant reduction of cell viability (B) and invasion capability (C) was observed in OAS1 knockdown cell line Bxpc-3 and Panc-1. More apoptosis was observed in OAS1 knockdown cell line Bxpc-3 and Panc-1 (D). The expression of OAS1 in pancreatic cancer can predict overall survival at 1 year (AUC=0.646), 2 years (AUC=0.723) or 3 years (AUC=0.734) (E). A survival prediction model for pancreatic cancer patients was created based on expression of OAS1 and pathological staging using the Cox model and visualized it using Nomogram plots (F, G). ns, no significance, *p<0.05, ***p<0.001.
Supplier Page from Abcam for Anti-OAS1 antibody