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An aberrant INSM1-dependent intermediate neuronal progenitor state drives tumorigenesis in a human stem cell model of glioblastoma

ABSTRACT: An aberrant INSM1-dependent intermediate neuronal progenitor state drives tumorigenesis in a human stem cell model of glioblastoma

PROVIDER: PRJNA956944 | ENA |

REPOSITORIES: ENA

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An aberrant INSM1-dependent intermediate neuronal progenitor state drives tumorigenesis in a human stem cell model of glioblastoma

Project description:Glioblastoma (GBM) is an aggressive, incurable brain tumor driven by heterogeneity between tumor cell-intrinsic and -extrinsic states for rapid evolution. To investigate how canonical GBM mutations promote functional plasticity, we developed an isogenic human neural stem cell (NSC) model of GBM by sequential addition of TERT promoter, TP53, and PDGFRA point mutations. TP53 loss-of-function increased TERT expression during serial mutagenesis, but only triple mutant NSCs reliably formed lethal in vivo tumors that recapitulate GBM. Tumor cell evolution began with stress-related metabolic changes and transitioned toward neuronal progenitor networks driven by transcription factor INSM1, which is highly expressed in human GBM tumors and intermediate progenitor cells during development that give rise to neuronal progenitors. Remarkably, inhibiting INSM1 in triple mutant NSCs caused reversal of oncogenic gene expression and functions to those of non-tumorigenic wildtype NSCs. These findings highlight the functional importance of an aberrant intermediate neuronal progenitor state in GBM pathogenesis.

2025-07-15 | GSE229901 | GEO

Aberrant EZHIP Expression Drives Tumorigenesis in Osteosarcoma

Project description:Aberrant EZHIP Expression Drives Tumorigenesis in Osteosarcoma

| PRJNA1006401 | ENA

Transcriptional regulation of endocrine cell differentiation by Insm1

Project description:This experiment used RNA-Seq technology to explore gene expression in mouse Insm1^GFP/Pdx1^CFP HIGH [het/het] FACS sorted pancreatic cells (pre-beta cells) and Insm1^GFP/Pdx1^CFP LOW [het/het] cells (other endocrine progenitors) at E15.5 and E18.5. Comparison of Insm1 +/Pdx HIGH and Insm1 +/Pdx LOW cells revealed a set of differentially expressed genes that are required for beta cell specification.

2014-07-01 | E-MTAB-1929 | biostudies-arrayexpress

Insm1 cooperates with Neurod1 and Foxa2 to maintain mature pancreatic β-cell function (Insm1, Neurod1 and Foxa2 ChipSeq data from pancreatic beta cell)

Project description:Genome-wide Insm1 binding sites analysis revealed an overrepresentation of sequences predicted to bind bHLH and/or forkhead factors, and further analyses demonstrated that most Insm1 sites in the genome are co-occupied by Neurod1 and Foxa2. Binding regions co-occupied by all three factors but not single Insm1 sites explained a significant fraction of gene expression changes in Insm1 mutant β-cells. Together, our data provide evidence that an Insm1, Neurod1 and Foxa2 network maintains a mature gene expression program in β-cells. 6 samples include, replicates of Insm1 and Foxa2, IgG pull down as a control

2015-03-31 | E-GEOD-54046 | biostudies-arrayexpress

Insm1 cooperates with Neurod1 and Foxa2 to maintain mature pancreatic β-cell function (Insm1, Neurod1 and Foxa2 ChipSeq data from pancreatic beta cell)

2015-03-31 | GSE54046 | GEO

Aberrant Cdk5 phosphorylates Mcm2 and promotes pituitary tumorigenesis

Project description:Aberrant Cdk5 phosphorylates Mcm2 and promotes pituitary tumorigenesis

| PRJNA912745 | ENA

Insm1 regulates the expression of thymic tissue-restricted antigens and the immune tolerance [RNA-seq]

Project description:Insm1, encoding a zinc finger protein, is expressed specifically in neuroendocrine cells. Recent study showed the first evidence of Insm1 expression in medullary thymic epithelial cells (mTEC). Here we investigated the expression and function of Insm1 in mTEC. Mutation of Insm1 resulted in decreased proportion of mTEChi although normal development of other types of thymic cells. We detected altered expression of a subset of tissue-restricted antigens (TRAs) and mild decreased expression of Aire and Fezf2 in Insm1 mutant mTEC. We further showed that Insm1 recognizes a DNA sequence which is similar to the CCCTC-Binding factor (CTCF) binding motif. Mutation of Insm1 altered CTCF binding genome widely and thus the expression of genes. In nude mice transplanted with Insm1 mutant thymus, autoimmune responses were observed in multiple peripheral tissues. In thymus specific Insm1 mutant mice, we detected decreased induction of regulatory T (Treg) cells in the thymus, obvious lymphocytes infiltration and autoimmune antibody reaction in several peripheral tissues. In thymic epithelial cells specific Insm1 overexpression mice, we detected enlarged mTEC proportion and increased expression of mTEC specific genes. Thus, we suggest that Insm1 is a novel regulator of mTEC function and autoimmunity.

2024-01-01 | GSE193927 | GEO

Insm1 regulates the expression of thymic tissue-restricted antigens and the immune tolerance [CUT&Tag]

2024-01-01 | GSE193926 | GEO

Insm1 cooperates with Neurod1 and Foxa2 to maintain mature pancreatic β-cell function (Expression data from islets of control and Insm1 conditional deleted adult pancreatic islets)

Project description:The zinc finger factor Insm1 is known to regulate differentiation of pancreatic β cells during development, Here we show that Insm1 is essential for the maintenance of functionally mature pancreatic β cells in mice. We used microarrays to analyse the global gene expression after deletion of insm1 in adult pancreatic β cells and identified functional important genes and immature islets releated genes deregulated in the mutatant islets.

2015-03-31 | GSE54044 | GEO

Insm1 cooperates with Neurod1 and Foxa2 to maintain mature pancreatic ?-cell function (Expression data from islets of control and Insm1 conditional deleted adult pancreatic islets)

Project description:The zinc finger factor Insm1 is known to regulate differentiation of pancreatic ? cells during development, Here we show that Insm1 is essential for the maintenance of functionally mature pancreatic ? cells in mice. We used microarrays to analyse the global gene expression after deletion of insm1 in adult pancreatic ? cells and identified functional important genes and immature islets releated genes deregulated in the mutatant islets. We used 8 mutant and 8 litter matched control mice for the islets preparation.

2015-03-31 | E-GEOD-54044 | biostudies-arrayexpress

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