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Identification of NOTCH3 unique target genes

ABSTRACT: Notch signaling is an evolutionarily conserved signaling pathway.NOTCH3 signaling has been shown to potentially paly an important role in luminal cell fate commitment in human breast tissue by regulating unique target genes We overexpressed the intracellular domain of NOTCH1 (N1ICD) and NOTCH3 (N3ICD) receptor in nonmalignant human breast cell line, 184-hTerts

ORGANISM(S): Homo sapiens

PROVIDER: GSE127236 | GEO | 2019/08/31

REPOSITORIES: GEO

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Non-overlapping functions for Notch1 and Notch3 during murine steady state thymic lymphopoiesis.

Project description:Notch1 signaling is absolutely essential for steady-state thymic lymphopoiesis, but the role of other Notch receptors, and their potential overlap with the function of Notch1, remains unclear. Here we show that like Notch1, Notch3 is differentially expressed by progenitor thymocytes, peaking at the DN3 progenitor stage. Using mice carrying a gene-trapped allele, we show that thymic cellularity is slightly reduced in the absence of Notch3, although progression through the defined sequence of TCR-αβ development is normal, as are NKT and TCRγδ cell production. The absence of a profound effect from Notch3 deletion is not explained by residual function of the gene-trapped allele, since insertion mapping suggests that the targeted allele would not encode functional signaling domains. We also show that although Notch1 and Notch3 are co-expressed on some early intrathymic progenitors, the relatively mild phenotype seen after Notch3 deletion does not result from the compensatory function of Notch1, nor does Notch3 function explain the likewise mild phenotype seen after conditional (intrathymic) deletion of Notch1. Our studies indicate that Notch1 and Notch3 carry out non-overlapping functions during thymocyte differentiation, and that while Notch1 is absolutely required early in the lymphopoietic process, neither receptor is essential at later stages.

2011-08-03 | GSE30631 | GEO

NOTCH3 Blockade Inhibits Cancer Cell Plasticity through a NOTCH3/PD-L1 Oncogenic Axis in Triple Negative Breast Cancer

Project description:Triple negative breast cancer (TNBC) accounts for 15-20% of all breast cancers and mainly affects pre-menopausal and minority women. Therapeutic options are yet limited, in part because of acquisition of tumor cells with cancer stem cell (CSC) properties, leading to intrinsic resistance to chemotherapeutic agents and immune evasion capacity. Dysregulated Notch signaling has been linked to breast cancer and in this study, we demonstrate the pivotal role of NOTCH3 in inducing the enrichment of chemoresistant ALDHhigh CSCs. Significantly, selective targeting of NOTCH3 with AV-353, a novel humanized monoclonal antibody, or by shRNA-mediated knockdown, impaired the enrichment of ALDHhigh CSCs with high self-renewal capacity, induced apoptosis and enhanced chemosensitivity. AV-353 treatment similarly reduced growth of xenografted tumors in vivo. Moreover, blocking NOTCH3 by AV-353 or shRNA reduced PD-L1 expression in TNBC cells, which was linked to the inhibition of tumor growth and enhancement of CD8+ T-cell infiltration. Taken together, these findings provide preclinical evidence for NOTCH3 as a novel therapeutic target in TNBC and reveal a novel NOTCH3/PD-L1 oncogenic axis as a platform for the betterment of TNBC therapy.

2024-06-28 | GSE236140 | GEO

The common oncogenomic program of NOTCH1 and NOTCH3 signaling in T-cell acute lymphoblastic leukemia [ChIP-seq]

Project description:Notch is a major oncogenic driver in T cell acute lymphoblastic leukemia (T-ALL), in part because it binds to an enhancer that increases expression of MYC. Here, we exploit the capacity of activated NOTCH1 and NOTCH3 to induce T-ALL, despite substantial divergence in their intracellular regions, as a means to elucidate a broad, common Notch-dependent oncogenomic program through systematic comparison of the transcriptomes and Notch-bound genomic regulatory elements of NOTCH1- and NOTCH3-dependent T-ALL cells. ChIP-seq studies show a high concordance of functional NOTCH1 and NOTCH3 genomic binding sites that are enriched in binding motifs for RBPJ, the transcription factor that recruits activated Notch to DNA. The interchangeability of NOTCH1 and NOTCH3 was confirmed by rescue of NOTCH1-dependent T-ALL cells with activated NOTCH3 and vice versa. Despite remarkable overall similarity, there are nuanced differences in chromatin landscapes near critical common Notch target genes, most notably at a Notch-dependent enhancer that regulates MYC, which correlates with responsiveness to Notch pathway inhibitors. Overall, a common oncogenomic program driven by binding of either Notch is sufficient to maintain T-ALL cell growth, whereas cell-context specific differences appear to influence the response of T-ALL cells to Notch inhibition.

2017-09-27 | GSE104261 | GEO

The common oncogenomic program of NOTCH1 and NOTCH3 signaling in T-cell acute lymphoblastic leukemia [expression array]

2017-09-27 | GSE104260 | GEO

Identification of NOTCH3 unique target genes

Project description:Identification of NOTCH3 unique target genes

| PRJNA524386 | ENA

Aberrant activation of canonical Notch1 signaling in the mouse prostate drives epithelialcell proliferation and induces prostatic hyperplasiaby increasing androgen receptor sensitivity

Project description:To investigate the regulatory role of Notch1 signaling pathway in mouse prostate growth and development, we constructed mice with prostate-specific overactivation of Notch1 intracellular domain N1ICD, in which Notch1 signaling was overactivated in prostate epithelial cells. We then analyzed gene expression profiles in the prostates of overexpressed and normal Notch1 mice.

2023-04-11 | GSE200565 | GEO

NOTCH3-IC

Project description:NOTCH3-IC

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Notch3 ChIP-sequencing of brain mural cells differentiated from human pluripotent stem cell-derived neural crest via Notch3 activation

Project description:Molecular mechanisms underlying the differentiation of brain mural cells from neural crest are poorly understood. We found that activation of Notch3 signaling in human pluripotent stem cell-derived neural crest (using lentiviral overexpression of the human Notch3 intracellular domain, N3ICD) was sufficient to direct the differentiation of mural cells. We used Notch3 ChIP-sequencing to identify cis-regulatory elements directly bound by the Notch3 transcriptional activation complex in this system.

2024-02-02 | GSE205212 | GEO

Identification of Notch1 regulated genes in A549 NSCLC cell line

Project description:Notch signaling is an evolutionarily conserved signaling pathway. Notch1 signaling has been shown to potentially paly an important role in cancer development and progression. To illustrate the underlying regulating mechanisms of Notch1 activation in NSCLC, the intracellular domain of Notch1 receptor (NICD1) was overexpressed in A549 cell line and the RNA-sequences were performed.

2019-09-30 | GSE137106 | GEO

Gene expression of skeletal muscles in response to overexpression of Notch1 intracellular domain (N1ICD)

Project description:Analysis of gene expression profile of Tibialis anterior (TA) skeletal muscle tissues with Notch1 intracellular domain (N1ICD) overexpression. Skeletal myogenesis involves sequential activation, proliferation, self-renewal/differentiation and fusion of myogenic stem cells (satellite cells). Notch signaling is known to be essential for the maintenance of satellite cells, but its function in late-stage myogenesis, i.e. post-differentiation myocytes and post-fusion myotubes, is unknown. Here we use muscle creatine kinase (MCK)-Cre to induce N1ICD expression in multinucleated myotubes. We found that myotube-specific Notch1 activation improved muscle regeneration and exercise performance of mdx mice, a model of Duchenne Muscular Dystrophy (DMD). Agilent microarray was performed to compare gene expression in mdx control and N1ICD-overexpressing mdx muscles. The results may provide mechanistic insights into how Notch1 activation in myotubes modulate muscle function.

2016-10-01 | GSE81242 | GEO

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