Context-dependent Regulation of Notch Signaling in Glial Development and Tumorigenesis [Bulk RNA-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1003000 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25548350_1.fastq.gz | Fastqsanger.gz | |||
| SRR25548350_2.fastq.gz | Fastqsanger.gz | |||
| SRR25548351_1.fastq.gz | Fastqsanger.gz | |||
| SRR25548351_2.fastq.gz | Fastqsanger.gz | |||
| SRR25548352_1.fastq.gz | Fastqsanger.gz |
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Project description:In the mammalian brain, Notch signaling maintains the cortical stem cell pool and regulates the glial cell fate choice and differentiation. However, the function of Notch in regulating glial development and its involvement in tumorigenesis have not been well understood. Here, we show that Notch inactivation by genetic deletion of Rbpj in stem cells decreases astrocytes but increases oligodendrocytes with altered internal states. Interestingly, inhibiting Notch in glial progenitors does not affect cell generation but instead accelerates the growth of Notch-deprived oligodendrocyte progenitor cells (OPCs), and OPC-related glioma. We also identified a crosstalk between oligodendrocytes and astrocytes, with premyelinating oligodendrocytes secreting Bmp4, which is repressed by Notch, to upregulate GFAP expression in adjacent astrocytes. Moreover, Notch inactivation in stem cells causes a glioma subtype shift from astroglia-associated to OPC-correlated patterns, and vice versa. Our study reveals Notch's context-dependent function, promoting astrocytes and astroglia-associated glioma in stem cells and repressing OPCs and related glioma in glial progenitors.
2023-08-12 | GSE240223 | GEO
Project description:In the mammalian brain, Notch signaling maintains the cortical stem cell pool and regulates the glial cell fate choice and differentiation. However, the function of Notch in regulating glial development and its involvement in tumorigenesis have not been well understood. Here, we show that Notch inactivation by genetic deletion of Rbpj in stem cells decreases astrocytes but increases oligodendrocytes with altered internal states. Interestingly, inhibiting Notch in glial progenitors does not affect cell generation but instead accelerates the growth of Notch-deprived oligodendrocyte progenitor cells (OPCs), and OPC-related glioma. We also identified a crosstalk between oligodendrocytes and astrocytes, with premyelinating oligodendrocytes secreting Bmp4, which is repressed by Notch, to upregulate GFAP expression in adjacent astrocytes. Moreover, Notch inactivation in stem cells causes a glioma subtype shift from astroglia-associated to OPC-correlated patterns, and vice versa. Our study reveals Notch's context-dependent function, promoting astrocytes and astroglia-associated glioma in stem cells and repressing OPCs and related glioma in glial progenitors.
2023-08-12 | GSE240222 | GEO
Project description:Context-dependent Regulation of Notch Signaling in Glial Development and Tumorigenesis
| PRJNA1002998 | ENA
Project description:Context-dependent Regulation of Notch Signaling in Glial Development and Tumorigenesis [scRNA-seq]
| PRJNA1003001 | ENA
Project description:Notch signaling regulates a variety of developmental cell fates decisions in a cell-context dependent manner. Although Notch signaling directly regulates transcription via the RBP-J/CSL DNA binding protein, little is known about the genes in the respective tissues that are directly activated by Notch. To analyze how Notch signaling mediates its context dependent functions, we utilized a Tamoxifen(OHT)-inducible system (NERT) to activate Notch1 in embryonic stem cells (ESC) at different stages of mesodermal differentiation combined with global transcriptional analyses. Notch1 signaling pathway was analysed in mouse embryonic stem cells (mESCs) that were kept under self-renewal conditions enabling ectodermal, or mesodermal gene expression (ESCe or ESCm respectively), or were differentiated into mesodermal progenitors. NotchIC were induced or not induced by hydroxytamoxifen (OHT) and addititionally in some experiments the cells were treated with protein synthesis inhibitor cycloheximide (CHX) for 4 h.
2010-07-13 | E-GEOD-15268 | biostudies-arrayexpress
Project description:Notch signaling regulates a variety of developmental cell fates decisions in a cell-context dependent manner. Although Notch signaling directly regulates transcription via the RBP-J/CSL DNA binding protein, little is known about the genes in the respective tissues that are directly activated by Notch. To analyze how Notch signaling mediates its context dependent functions, we utilized a Tamoxifen(OHT)-inducible system (NERT) to activate Notch1 in embryonic stem cells (ESC) at different stages of mesodermal differentiation combined with global transcriptional analyses.
2010-07-13 | GSE15268 | GEO
Project description:The Notch signaling pathway regulates fate decision, proliferation and differentiation of intestinal epithelial cells. However, the role of Notch signaling in colorectal cancer progression is largely unknown. Here we show that Notch signaling suppresses the progression of colorectal tumorigenesis, even though it augments tumor initiation. In contrast to adenomas of Apcmin mice, Notch-inactivated Apcmin adenomas showed more malignant characteristics, such as submucosal invasion and loss of glandular pattern. Conversely, Notch-activated Apcmin adenomas showed a reversion from high-grade to low-grade features, such as the restoration of adherent junctions. Expression profiling revealed that Notch signaling promotes the differentiation of tumor cells with down regulation of Wnt/beta-catenin target genes and inhibition of epithelial-mesenchymal transition. Comparison of mouse and human expression profiles also suggests the common role of Notch in inhibition of tumor progression. Interestingly, Notch signaling suppressed the expression of beta-catenin responsive genes through chromatin modification of Tcf4/beta-catenin binding sides. Our results suggest that Notch signaling has dual roles in colorectal tumorigenesis: promoting adenoma initiation, while inhibiting tumor progression to colorectal cancer. mRNAs from normal (WT, Notch-activated and Notch-inactivated) and tumor (WT, Notch-activated and Notch-inactivated) tissues were profiled.
2011-04-19 | E-GEOD-21392 | biostudies-arrayexpress
Project description:In the mammalian brain, Notch signaling maintains the cortical stem cell pool and regulates the glial cell fate choice and differentiation. However, the function of Notch in regulating glial development and its involvement in tumorigenesis have not been well understood. Here, we show that Notch inactivation by genetic deletion of Rbpj in stem cells decreases astrocytes but increases oligodendrocytes with altered internal states. Inhibiting Notch in glial progenitors does not affect cell generation but instead accelerates the growth of Notch-deprived oligodendrocyte progenitor cells (OPCs) and OPC-related glioma. We also identified a cross-talk between oligodendrocytes and astrocytes, with premyelinating oligodendrocytes secreting BMP4, which is repressed by Notch, to up-regulate GFAP expression in adjacent astrocytes. Moreover, Notch inactivation in stem cells causes a glioma subtype shift from astroglia-associated to OPC-correlated patterns and vice versa. Our study reveals Notch's context-dependent function, promoting astrocytes and astroglia-associated glioma in stem cells and repressing OPCs and related glioma in glial progenitors.
| S-EPMC10637744 | biostudies-literature
Project description:The Notch signaling pathway regulates fate decision, proliferation and differentiation of intestinal epithelial cells. However, the role of Notch signaling in colorectal cancer progression is largely unknown. Here we show that Notch signaling suppresses the progression of colorectal tumorigenesis, even though it augments tumor initiation. In contrast to adenomas of Apcmin mice, Notch-inactivated Apcmin adenomas showed more malignant characteristics, such as submucosal invasion and loss of glandular pattern. Conversely, Notch-activated Apcmin adenomas showed a reversion from high-grade to low-grade features, such as the restoration of adherent junctions. Expression profiling revealed that Notch signaling promotes the differentiation of tumor cells with down regulation of Wnt/beta-catenin target genes and inhibition of epithelial-mesenchymal transition. Comparison of mouse and human expression profiles also suggests the common role of Notch in inhibition of tumor progression. Interestingly, Notch signaling suppressed the expression of beta-catenin responsive genes through chromatin modification of Tcf4/beta-catenin binding sides. Our results suggest that Notch signaling has dual roles in colorectal tumorigenesis: promoting adenoma initiation, while inhibiting tumor progression to colorectal cancer.
2011-04-19 | GSE21392 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2023-08-12 | GSE240224 | GEO