Loss of Egr1 promotes tumor progression, immune modulation, and differential gene expression in Kras-driven lung cancer. (IMAGE)
Caption
(A) Schematic illustration of the experimental design for Egr1 knockout versus control. KC mice were administered a pool of two sgRNAs targeting Egr1 (n = 3) or a pool of control sgInerts (n = 3).
(B) Representative images of lung lobes from mice at 20 weeks after tumor initiation via Lenti-sgEgr1-pool/Cre or Lenti-sgInerts. Images include fluorescence views under a dissecting microscope, hematoxylin-eosin-stained sections, TTF1-stained sections to confirm lung adenomatous origin, and Egr1 staining to confirm knockout efficiency.
(C) Bulk RNA-sequencing analysis was conducted on lung tissues at 20 weeks after tumor initiation in Egr1 knockout and control mice. The left panel displays a heatmap of 421 differentially expressed genes (DEGs) identified with a false discovery rate-adjusted P-value < 0.05, illustrating two distinct expression clusters. The right panel highlights a heatmap of the top 50 most deregulated genes, showing clear differences between the two groups.
(D) Gene Ontology analysis was performed using Metascape on significantly up-regulated genes between Egr1 knockout and control mice. Statistically enriched terms were identified based on cumulative hypergeometric P-values and enrichment scores. The top 20 most significant terms, predominantly associated with immune processes, are visualized.
Credit
Athar Khalil, Trang Dinh, Meaghan Parks, Rebecca C. Obeng, Berkley Gryder, Adam Kresak, Yuxiang Wang, Jeff Maltas, Madeline Bedrock, Xiangzhen Wei, Zachary Faber, Mira Rahm, Jacob Scott, Thomas LaFramboise, Zhenghe Wang, Christopher McFarland
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