Fig. 6: INSM1 is upregulated in human GBM tumors and is critical for in vivo tumorigenicity.
From: INSM1 governs a neuronal progenitor state that drives glioblastoma in a human stem cell model
A INSM1 expression in TCGA-GBM bulk RNA-seq data vs. normal brain (left, Student’s t test, two-sided, **P < 0.01) and GBM bulk classification (right, ANOVA, ****P < 0.001). B INSM1 expression in scRNA-seq data from 28 GBM patient tumors10. Dimension reduction by cell state hierarchy as defined in Neftel et al.10. C Single cell RNA-seq analysis of a PRO human GBM colored by RNA velocity latent time (left) and clustered subpopulations (right). Shown is the UMAP reduction based on RNA splicing kinetics (Dynamo22). D Expression of key INSM1-related genes from PRO eNSCs in PRO human GBM clusters ordered by RNA content trajectory inference. E Kaplan-Meier survival analysis of mice orthotopically implanted with PRO eNSCs (clones 1 + 2) following lentiviral transduction of two independent INSM1 RNAi (INSM1i) or control RNAi (shCtrl) (clone 1: n = 10; clone 2: n = 5, log-rank, ****P < 0.0001). F Representative T2-weighted MRI images of mice from each experimental cohort 200 days post-xenograft with RNAi-transduced PRO eNSCs. Red outlines indicate pathological lesions in the coronal plane of the injection site (scale bar = 1 mm; L = left, P = posterior, R = right). Source data are provided as a Source Data file, including exact statistical analyses and p values.
