Fig. 5: INSM1 inhibition in PRO eNSCs induces metabolic and developmental regression.
From: INSM1 governs a neuronal progenitor state that drives glioblastoma in a human stem cell model
A Expression of INSM1, TCF4, or SOX4 mRNA by qRT-PCR normalized to ACTIN and GAPDH expression in PRO eNSCs following inhibition by RNA interference (RNAi). Data represent mean ± SEM in independent replicates (INSM1i and TCF4i: n = 3; SOX4i: n = 4, Student’s t test, two-sided, ****P < 0.0001). B Single cell transcriptomic profiling of PRO eNSCs following TF inhibition. Shown is the integrated PCA-guided UMAP embedding colored by combined RNAi labels (left) and individual RNAi labels (right). C Spearman similarity correlation between shCtrl and TF RNAi in PRO eNSCs by pseudobulk analysis of top variable features. D PRO eNSC INSM1i PCA-based UMAP. E Gene ontology of PRO eNSC INSM1i differentially expressed genes (n = 257). Circle size represents number of genes within each ontology, and color indicates log-transformed FDR. F Spearman similarity correlation between WT, PRO, and INSM1i eNSC by pseudobulk analysis of top variable features. G Proportions of GBM functional cell state labeling in WT, PRO, and INSM1i eNSCs (GPM: glycolytic/plurimetabolic, MTC: mitochondrial, NEU: neuronal, PPR: proliferating progenitor). H Seahorse XF analysis of glycolysis-dependent extracellular acidification rate in PRO eNSCs following inhibition of INSM1 using two independent RNAi. Data represent mean ± SEM in independent replicates (n = 4, ANOVA, ****P < 0.0001). I Seahorse XF analysis of glycolysis-dependent extracellular acidification rate in B67 primary GSCs following inhibition of INSM1 using two independent RNAi (GIPZ RNAi, Methods). Data represent mean ± SEM in independent replicates (n = 6, ANOVA, *P < 0.05, **P < 0.01). Source data are provided as a Source Data file, including exact statistical analyses and p values.
