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Fig. 1 | Journal of Experimental & Clinical Cancer Research

Fig. 1

From: Metabolic synthetic lethality by targeting NOP56 and mTOR in KRAS-mutant lung cancer

Fig. 1

NOP56 confers a metabolic dependency in KRAS-mutant cancers. A, Venn diagram showing common essential genes in KRAS-mutant cancer cells. Data are based on the published studies, with the 21 common genes listed on the right. B, Network analysis of the 21 common genes by STRING. C, NOP56 mRNA expression in KRAS-mutant lung cancer (LC), pancreatic cancer (PC) and colon cancer (CC) versus KRAS-wild-type (WT) cancers in patient samples from TCGA. D, Prognostic values of NOP56 expression across TCGA lung adenocarcinoma (left), pancreatic cancer (middle) and colon cancer (right) cohorts harboring KRAS mutations. Kaplan–Meier survival analyses were stratified by the optimal cut-off value of NOP56 mRNA levels. E, Gene set enrichment analysis (GSEA) revealed significant enrichment of oxidative phosphorylation and ROS pathway gene signatures in NOP56-depleted KRAS-mutant cancer cells (SW480). The GEO dataset GSE15212 was used for GSEA. F, H358 and H460 cells transfected with NOP56-specific or control siRNAs were treated (72 h post-transfection) with 300 μM H2O2 for 6 h, followed by incubation with H2DCFDA for 30 min, and analyzed by flow cytometry. Quantification of relative ROS levels was shown in the right. Data are shown as the mean ± SD (n = 3). *P < 0.05,***P < 0.001, ****P < 0.0001 by two-way ANOVA with Tukey’s multiple comparisons test. G, H358 and H460 cells transfected with NOP56-specific or control siRNAs were subsequently (72 h post transfection) treated with vehicle (DMSO) or 300 μM H2O2 for 6 h before apoptotic assay. Data were shown as mean ± SD (n = 3). *P < 0.05 and ***P < 0.001 by two-way ANOVA with Tukey’s multiple comparisons test

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