Research Paper Volume 15, Issue 21 pp 12136—12154

Figure 8. The potential downstream targets of PUS1. (A) The intersection analysis of the GSEA analysis in LUAD and LUSC between high– and low–PUS1 expression patients using hallmark gene sets; (B) GSEA analysis revealed that DNA_REPAIR, E2F_TARGETS, MYC_TARGETS_V2, G2M_CHECKPOINT, and MYC_TARGETS_V1 were significantly enriched in patients with high PUS1 expression, and TGF_BETA_SIGNALING, UV_RESPONSE_DN were significantly enriched in patients with low PUS1 expression in LUAD; (C) GSEA analysis revealed that DNA_REPAIR, E2F_TARGETS, MYC_TARGETS_V2, G2M_CHECKPOINT, and MYC_TARGETS_V1 were significantly enriched in patients with high PUS1 expression, and TGF_BETA_SIGNALING, UV_RESPONSE_DN were significantly enriched in patients with low PUS1 expression in LUSC; (D) The intersection analysis in DNA_REPAIR, E2F_TARGETS, MYC_TARGETS_V2, G2M_CHECKPOINT and MYC_TARGETS_V1 gene sets; (E, F) The correlation analysis between PUS1 expression and NOLC1, CDK4, MCM5, and MYC in LUAD and LUSS based on CPTAC dataset; (G) The intersection analysis in PUS1_dep_Ψsite, PUS1_LUAD_cor, and A549_ Ψ site; (H) The correlation analysis between PUS1 expression and XPO1 in LUAD based on CPTAC dataset. (I) The expression of NOLC1, MCM5, MYC, and XPO1 mRNA expression after knockdown of PUS1 in A549 cells. ^*P < 0.05, ^**P < 0.01, ^***P < 0.001.