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Receptor tyrosine kinase signaling promotes post-embryonic morphogenesis and survival of glia and neural progenitor cells

ABSTRACT: Receptor tyrosine kinase signaling promotes post-embryonic morphogenesis and survival of glia and neural progenitor cells

PROVIDER: PRJNA506003 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8206640_1.fastq.gz	Fastqsanger.gz
	SRR8206640_2.fastq.gz	Fastqsanger.gz
	SRR8206631_1.fastq.gz	Fastqsanger.gz
	SRR8206631_2.fastq.gz	Fastqsanger.gz
	SRR8206632_1.fastq.gz	Fastqsanger.gz

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Receptor tyrosine kinase signaling promotes post-embryonic morphogenesis and survival of glia and neural progenitor cells

Project description:Glioblastomas (GBMs), which are the most deadly malignant brain tumors of children and adults, infiltrate the brain and grow rapidly, and are resistant to current therapies. Glioblastomas (GBMs) frequently display mutations that activate receptor tyrosine kinases (RTKs), such as EGFR, which are thought to cooperate with additional factors to drive tumorigenesis. To identify and characterize genetic pathways that cooperate with RTKs to drive GBM progression, we performed RNA sequencing on several cell cultures created from surgical specimens from tumors with alterations in RTKs, and these cultures were grown as neurospheres in serum-free media used for normal neural stem/progenitor cell cultures. Under these conditions, GBM cells retain many defining features and mutations found in primary tumors. For comparison, we profiled commercially available human normal neural stem cells (HNPCs), which were grown under the same conditions. Data from these cell cultures was analyzed for transcripts differentially expressed between GBM cells and HNPCs, which showed that GBM cells that show RTK alterations strongly overexpressed the PDGFA and IGF2 secreted factors, which likely cooperate with EGFR to drive tumor progression.

2018-11-20 | GSE122679 | GEO

Tyrosine Kinase Inhibitor Cardiotoxicity

Project description:Tyrosine Kinase Inhibitor Cardiotoxicity

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Pvr receptor tyrosine kinase signaling promotes post-embryonic morphogenesis, and survival of glia and neural progenitor cells in Drosophila.

Project description:Stem cells reside in specialized microenvironments, called niches, that regulate their development and the development of their progeny. However, the development and maintenance of niches are poorly understood. In the Drosophila brain, cortex glial cells provide a niche that promotes self-renewal and proliferation of neural stem cell-like cells (neuroblasts). In the central brain, neuroblasts and their progeny control post-embryonic morphogenesis of cortex glia through PDGF-like ligands, and this PDGFR receptor tyrosine kinase (RTK) signaling in cortex glia is required for expression of DE-cadherin, which sustains neuroblasts. Thus, through an RTK-dependent feed-forward loop, neuroblasts and their glial niche actively maintain each other. When the EGFR RTK is constitutively activated in cortex glia, they overexpress PDGF orthologs to stimulate autocrine PDGFR signaling, which uncouples their growth and survival from neuroblasts, and drives neoplastic glial transformation and elimination of neuroblasts. These results provide fundamental insights into glial development and niche regulation, and show that niche-neural stem cell feed-forward signaling becomes hijacked to drive neural tumorigenesis.

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Genetic control of cellular morphogenesis in Müller glia

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Fms-like tyrosine kinase 3 (Flt3) contributes to a receptor tyrosine kinase signature regulating the cardiac side population

Project description:Fms-like tyrosine kinase 3 (Flt3) contributes to a receptor tyrosine kinase signature regulating the cardiac side population

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Fms-like tyrosine kinase 3 (Flt3) contributes to a receptor tyrosine kinase signature regulating the cardiac side population

Project description:Fms-like tyrosine kinase 3 (Flt3) is a regulator of hematopoietic progenitor cells. It is a target of tyrosine kinase inhibitors (TKIs) used for acute myeloid leukemia treatment. Flt3 and its ligand (Flt3L) are expressed in the heart and cardiac side effects occur under Flt3-targeting TKIs. Whether Flt3/Flt3L also regulate cardiac progenitor cells (CPCs), however, is not known. The cardiac side population (SP) is a pool of heterogenous CPCs that can give rise to all cardiac lineages, hence contributing to cardiovascular homeostasis. Here we show that SP-CPCs produce and are responsive to Flt3L. Compared to wild-type, SP-CPCs from flt3L-/- mice are less abundant, with less contribution of CD45-CD34+ cells, and lower expression of gene sets related to epithelial-to-mesenchymal transition, cardiovascular development and stem cell differentiation. Upon culturing and compared to wild-type, flt3L-/- Sca1+CD31- SP-CPCs show increased proliferation and less vasculogenic commitment, but differentiation can be induced in the presence of receptor tyrosine kinase-activating growth factors. The observed differences are associated with decreased microvascularisation and global systolic function of flt3L-/- hearts. Thus, Flt3 contributes to a receptor tyrosine kinase signature necessary for the maintenance and functionality of SP-CPCs. These findings have potential implications regarding cardiovascular side effects observed under TKI therapy.

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Histologic transformation induced by EGFR tyrosine kinase inhibitors

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Yes tyrosine kinase signaling promotes liver cancer development

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Proteomic profiling by array of tyrosine kinase activity in metastatic malignant melanoma from human tissue specimens

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Project description:Yes tyrosine kinase signaling promotes liver cancer development [DSP294_SNU387]

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