Fig 1: The risk signature in HCC from the training set, the independent external validation cohort. (A, C) The Kaplan–Meier curves of the MAPK-RAP1A related risk signature. (B, D) Time-dependent ROC curves at 1, 3, and 5 years. AUC, area under the ROC; HCC, hepatocellular carcinoma; ROC, receiver-operating characteristic.
Fig 2: Rap1A knockdown attenuates tumor metastasis in vivo. (A) Images of ECA109 tumors using cells that stably expressed sh-NC or shRap1A. (B) Quantitative analysis of the tumor volume with the time lapse from day 7 onwards; error bars represent mean + 95% confidence intervals, n=6 mice/group. (C) An illustrative diagram of lungs extracted 6 weeks after ECA109-sh-NC or shRap1A were injected into the tail veins of nude mice. (D) Quantitative analysis of the metastatic nodules in the lungs; error bars represent the mean ± standard error of the mean; ***P<0.001. (E and F) Representative lung sections from each group and corresponding H&E staining [(E) magnification, ×5 and ×50] and IHC staining [(F) magnification, ×50 and ×200] for Rap1A. Rap1A, Ras-associated protein 1A; H&E, hematoxylin and eosin; IHC, immunohistochemistry.
Fig 3: Effect of the risk signature and immune checkpoint gene expression on patient survival. (A) Association between the risk signature and immune checkpoint gene expression. (B) Association between the hub gene and immune checkpoint gene expression. (C) Immunohistochemical staining was used to compare the expression of PGF, STMN1, ANGPT2, FLT3, RAP1A, HSPA8 with B7 in HCC tissues. (D) Kaplan–Meier survival curves of OS among patient groups stratified by the risk signature and immune checkpoint gene expression. (E) Association between B7 (CD80) and PDL1 in HCC tissues compared with adjacent tissues. Supplemental Figure Immunohistochemistry was used to detect the negative control, high and low expression of PGF, STMN1, ANGPT2, FLT3, RAP1A, HSPA8, and B7 in HCC tissues at high and low magnification.
Fig 4: SOCS1 inhibits the expression of Rap1a and activation of the JAK2/STAT2 pathway in macrophage inflammation induced by homocysteine.A Western blot analysis of Rap1a, p-JAK2, p-STAT2, and SOCS1 in Ad-FABP4 macrophages transfected with si-Rap1a and/or si-SOCS1 and treated with Hcy (n = 3). B The concentrations of IL-1β, IL-6, and TNF-α were analyzed by ELISA in macrophages as described above (n = 3). Data are expressed as the mean ± SD. *P < 0.05 versus Ad-FABP4 + si-NC + Hcy group; #P < 0.05 versus Ad-FABP4 + si-Rap1a+Hcy group.
Fig 5: Validation of immune estimate in the MAPK-RAP1A dataset. (A) The corresponding stromal score, immune score, and estimated score of MAPK-RAP1A gene signature between low-immunity group and high-immunity group. (B) Scores of stromal, immune, and ESTIMATE in HCC samples with different TNM stages. (C) Scores of stromal, immune, and ESTIMATE in HCC samples with different T stages. (D) Scores of stromal, immune, and ESTIMATE in HCC samples with different N stages. (E) Scores of stromal, immune, and ESTIMATE in HCC samples with different M stages.
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