Fig. 6
From: A novel mechanism for A-to-I RNA-edited CYP1A1 in promoting cancer progression in NSCLC

CYP1A1_I462V showed increased tolerance to oxidative stress in NSCLC. A KEGG pathways of differentially expressed proteins (DEPs) in A549I462V. B Heatmap illustrating the top 15 DEPs in A549I462V, as determined by proteome profile analysis. C Cells stained with 10 μM DCF-DA and analyzed by flow cytometry. Green panel: A549; orange panel: A549I462V; red panel treated with 1 μM OXA; blue panel: A549I462V treated with 1 μM OXA. D ROS generation was analyzed by Fluorence microplate reader. All results expressed as mean ± SEM of three independent experiments. *p < 0.05; ***p < 0.001. E Venn diagram comparing A549I462V − upregulated proteins, oxidative stress responsive proteins, and the target genes of the oxidative stress-related transcription factors Nrf2 and AP-1. F Protein–protein interaction (PPI) network of CYP1A1 and the upregulated protein signature as indicated