Fig 1: Stratification Analysis and Mutation landscape of high/low SLC11A1 subgroups. High SLC11A1 expression predicts poor prognosis in gliomas with different clinical characteristics. Patients were divided into high and low expressed group by the medium expression level. Kaplan-Meier plots of SLC11A1 were performed with a variety of clinical characteristics. (A) tumor grade, (B) IDH mutational status, (C) 1p/19q co-deletion, and (D) Age. (E) Oncoplots showed the top 20 genes of mutations in patients with high expression of SLC11A1. (F) Fishplot showed that with SLC11A1’s expression changing from high to low, IDH1 mutations progressively account for the dominant type of total mutations. (Q: quartile) (G) Violin plot showed higher tumor mutation burdens in patients with high SLC11A1 expression compared to those with low SLC11A1 expression.
Fig 2: Pan-cancer analysis of SLC11A1 expression. (A) UCSCXenaShiny was used to visualize SLC11A1 expression in the cancer genome atlas (TCGA) pan-cancer datasets. (B) Risk plot of correlation SLC11A1 with OS, PFI, DSS (red represents HR > 1(risky) and P value < 0.05; blue represents HR < 1 (protective) and P value < 0.05; grey represents no statistical significance). **,P < 0.01; ***,P < 0.001; ****,P < 0.0001, ns = no significance (Wilcoxon test).
Fig 3: Expression of SLC11A1 increased with the progression of glioma. (A) Univariate and multivariate analysis for overall survival of glioma patients. (B) CGGA, (C) TCGA, (D) Rembrandt, (E) GSE16011, (F) GSE4412, and (G) GSE43289. (The X-axis represents the WHO grade while the Y-axis represents SLC11A1 expression value (log2). Based on Wilcoxon test.) (H) qRT-PCR of SLC11A1 of 20 patients with gliomas. (I) Representations and quantification of immunohistochemistry detection of SLC11A1 in LGG (low grade glioma) and HGG (high grade glioma). *,P < 0.05; **,P < 0.01; ***,P < 0.001, ns = no significance (Wilcoxon test). (J) Western blot of SLC11A1 in LGG (low grade glioma) and HGG (high grade glioma).
Fig 4: SLC11A1 expression implies TME in gliomas. (A) Analysis of immune cell infiltration and SLC11A1’s specific expression through single cell data of gliomas. (B) Correlation between the SLC11A1’s expression and Mono/Macro cells (C) Analysis of SLC11A1’s location in gliomas based on spatial transcriptome. (D) Correlation between the SLC11A1’s expression and T-cell inflammatory signature. (E) Representative immunofluorescence images of human glioma samples co-stained with PDCD1 or CD68 (red) and SLC11A1 (green) in LGG and HGG. (F) Kaplan-Meier plots were performed in context of monocytes/macrophages infiltration and SLC11A1 expression. ***,P < 0.001 (Wilcoxon test). (G) Rates of anti-PD1 responses of patients from the CGGA cohort in the high or low SLC11A1 subgroups based on ImmunCellAI.
Fig 5: Subgroup divided by SLC11A1 predict potential immunotherapy responses of gliomas and identification of candidate agents with higher drug sensitivity in glioma patients. (E) Comparison of estimated olaparib (up) and temozolomide’s (down) sensitivity (logAUC) between IDH mutant and wildtype groups. (F) Comparison of estimated temozolomide’s sensitivity (logAUC) between high-SLC11A1 and low-SLC11A1 groups. (G) Spearman’s correlation analysis of three CTRP-derived compounds (up) and ten PRISM-derived compounds (down).
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