Fig. 3: Antagonizing function of MEN1 and MLL1 in regulating cytokine gene signature and TME infiltration. | Nature Genetics

Fig. 3: Antagonizing function of MEN1 and MLL1 in regulating cytokine gene signature and TME infiltration.

From: In vivo CRISPR screens identify a dual function of MEN1 in regulating tumor–microenvironment interactions

Fig. 3

a, RT–qPCR performed in A549 cells with and without MEN1 deletion coupled with deletion of MAVS and/or cGAS. Mean ± s.e.m. of two biological replicates is shown (unpaired two-tailed Student’s t-test). *P < 0.05, **P < 0.01. b, A549 xenograft tumor growth rate in immunodeficient mice with and without knockout of MEN1 or in combination with MAVS and/or cGAS knockout. Each data point represents mean ± s.e.m. tumor volumes (n = 10 for each arm). Two-way ANOVA was used for statistical analysis. ***P < 0.001, ****P < 0.0001. c, Dot plot showing enriched KEGG terms of mouse differential genes from MEN1 knockout A549 xenografts. d, Quantification of neutrophil infiltration in A549 xenograft tumors with and without MEN1 deletion. Mean ± s.e.m. of neutrophil percentage from 12 tumors is shown (unpaired two-tailed Student’s t-test). e, IHC staining showing percentage of neutrophil or CD8+ T cells in MEN1-high versus MEN1-low tumor samples from a LUAD microarray (TMA). Mean ± s.e.m. of 20 tumors with the highest and the lowest MEN1 TMA scores were assigned to each group. **P < 0.01, ***P < 0.001. f, Representative IHC staining images for MEN1, myeloperoxidase (neutrophil) and CD8 (CD8+ T cell). Scale bars, 200 μm. g, A549 xenograft tumor growth rate in immunodeficient mice with and without knockout of MEN1 or in combination with anti-Ly6G antibody injection. Each data point represents mean ± s.e.m. tumor volumes (n = 5 for each arm). Two-way ANOVA was used for statistical analysis. OR, odds ratio.

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