PROM1(CD133)-dependent expressed genes from mouse embryonic DRG neurons
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA622574 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11467728.fastq.gz | Fastqsanger.gz | |||
| SRR11467729.fastq.gz | Fastqsanger.gz | |||
| SRR11467730.fastq.gz | Fastqsanger.gz | |||
| SRR11467731.fastq.gz | Fastqsanger.gz |
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Project description:Prom1, also knwon as CD133 is a stem cell marker that are down-regulated during developmental process. Here we first reports that PROM1 is a regulator of expression of specific sets of genes from DRG neurons.
2020-04-02 | GSE147936 | GEO
Project description:Among pediatric acute lymphoblastic leukemias (ALL), KMT2A-rearranged infant ALL (KMT2Ar iALL) carries a particularly poor prognosis due to high rates of treatment-refractory or relapsing disease. Mechanistically, KMT2Ar drives aggressive disease through epigenetic dysregulation of multiple genes as a direct effect of expression of KMT2A-fusion proteins, most commonly KMT2A::AFF1, in leukemic cells. We previously showed that one of the top 2 most dysregulated genes, PROM1 (Prominin-1), encodes the cell surface protein prominin-1/CD133 and that this is essential for proliferation of KMT2A::AFF1+ cell lines. Here we show that PROM1 gene expression and cell surface CD133 expression specifically mark a highly proliferative subset of KMT2A::AFF1 blasts both in primary patient samples and in our highly physiologically relevant, primary human fetal liver HSPC-derived KMT2A::AFF1 ALL model (CRISPRKMT2A::AFF1 ALL). CD133+ CRISPRKMT2A::AFF1 blasts, but not CD133- CRISPRKMT2A::AFF1 blasts, exhibit a stem-cell gene expression profile and drive more aggressive disease in vivo. Furthermore, CRISPR-mediated inactivation of PROM1 reduces leukemic proliferation and prolongs survival of mice transplanted with CRISPRKMT2A::AFF1 blasts. These data show that PROM1/CD133 expression has an important functional role in CRISPRKMT2A::AFF1 ALL, and supports targeting PROM1/CD133 by pharmacological or immunotherapy-based approaches in KMT2A::AFF1 iALL.
2025-10-01 | GSE278786 | GEO
Project description:MLL gene rearrangements (MLLr) are a common cause of aggressive, incurable acute lymphoblastic leukemias (ALL) in infants and children, most of which originate in utero. The most common MLLr produces an MLL-AF4 fusion protein. MLL-AF4 promotes leukemogenesis by activating key target genes, mainly through recruitment of DOT1L and increased histone H3 lysine 79 methylation (H3K79me2/3). One key MLL-AF4 target gene is PROM1 which encodes CD133 (Prominin-1). CD133 is a pentaspan transmembrane glycoprotein that represents a potential pan-cancer target as it is found on multiple cancer stem cells. Here we demonstrate that aberrant PROM1/CD133 expression is essential for leukemic cell growth, mediated by direct binding of MLL-AF4. Activation is controlled by an intragenic H3K79me2/3 enhancer element (KEE) leading to increased enhancer-promoter interactions between PROM1 and the nearby gene TAPT1. This dual locus regulation is reflected in a strong correlation of expression in leukemia. We find that in PROM1/CD133 non-expressing cells, the PROM1 locus is repressed by polycomb repressive complex 2 (PRC2) binding, associated with reduced expression of TAPT1, partially due to loss of interactions with the PROM1 locus. Together, these results provide the first detailed analysis of PROM1/CD133 regulation that explains CD133 expression in MLLr ALL.
2020-03-25 | GSE135023 | GEO
Project description:MLL gene rearrangements (MLLr) are a common cause of aggressive, incurable acute lymphoblastic leukemias (ALL) in infants and children, most of which originate in utero. The most common MLLr produces an MLL-AF4 fusion protein. MLL-AF4 promotes leukemogenesis by activating key target genes, mainly through recruitment of DOT1L and increased histone H3 lysine 79 methylation (H3K79me2/3). One key MLL-AF4 target gene is PROM1 which encodes CD133 (Prominin-1). CD133 is a pentaspan transmembrane glycoprotein that represents a potential pan-cancer target as it is found on multiple cancer stem cells. Here we demonstrate that aberrant PROM1/CD133 expression is essential for leukemic cell growth, mediated by direct binding of MLL-AF4. Activation is controlled by an intragenic H3K79me2/3 enhancer element (KEE) leading to increased enhancer-promoter interactions between PROM1 and the nearby gene TAPT1. This dual locus regulation is reflected in a strong correlation of expression in leukemia. We find that in PROM1/CD133 non-expressing cells, the PROM1 locus is repressed by polycomb repressive complex 2 (PRC2) binding, associated with reduced expression of TAPT1, partially due to loss of interactions with the PROM1 locus. Together, these results provide the first detailed analysis of PROM1/CD133 regulation that explains CD133 expression in MLLr ALL.
2020-03-25 | GSE135025 | GEO
Project description:MLL gene rearrangements (MLLr) are a common cause of aggressive, incurable acute lymphoblastic leukemias (ALL) in infants and children, most of which originate in utero. The most common MLLr produces an MLL-AF4 fusion protein. MLL-AF4 promotes leukemogenesis by activating key target genes, mainly through recruitment of DOT1L and increased histone H3 lysine 79 methylation (H3K79me2/3). One key MLL-AF4 target gene is PROM1 which encodes CD133 (Prominin-1). CD133 is a pentaspan transmembrane glycoprotein that represents a potential pan-cancer target as it is found on multiple cancer stem cells. Here we demonstrate that aberrant PROM1/CD133 expression is essential for leukemic cell growth, mediated by direct binding of MLL-AF4. Activation is controlled by an intragenic H3K79me2/3 enhancer element (KEE) leading to increased enhancer-promoter interactions between PROM1 and the nearby gene TAPT1. This dual locus regulation is reflected in a strong correlation of expression in leukemia. We find that in PROM1/CD133 non-expressing cells, the PROM1 locus is repressed by polycomb repressive complex 2 (PRC2) binding, associated with reduced expression of TAPT1, partially due to loss of interactions with the PROM1 locus. Together, these results provide the first detailed analysis of PROM1/CD133 regulation that explains CD133 expression in MLLr ALL.
2020-03-25 | GSE135024 | GEO
Project description:As many other tumors, a subset of gliobastoma is thought to be maintained by a restricted population of cancer cells, stem-like cells that express CD133 transmembrane protein. Expression levels of CD133 gene has been linked to a poor prognostic molecular subgroup and is not overexpressed by the PDGF-driven proneural group. Thus, the significance of CD133+ cells for gliomagenesis of the proneural group is undetermined. In addition, the role of the CD133 protein remains elusive and controversial, which results from the difficult isolation of CD133+ cells that has largely relied on the use of antibodies to ill-defined glycosylated epitopes of CD133. Here, we used a knockin lacZ reporter mouse, Prom1lacZ/+, to track Prom1+ cells in the brain and found that Prom1 (prominin1, murine CD133 homologue) is expressed by cells that co-express markers characteristic of neuronal, glial and vascular lineage phenotype. In proneural tumors derived from injection of RCAS-PDGF into the brain of tv-a;Ink4a-Arf-/- Prom1lacZ/+ mice, Prom1+ cells co-express markers for astrocytes and endothelial cells. Therefore, we characterize the tumor propagation in a murine model and found that the mice co-transplanted with Prom1 endothelium and proneural tumor spheres cells had significant tumor burden and vascular proliferation (angiogenesis). Specific genes in Prom1 endothelium are identified that code for endothelial signaling modulators that most likely support proneural tumor progression and can be potential targets for anti-angiogenic therapy.
2013-12-31 | GSE43931 | GEO
Project description:As many other tumors, a subset of gliobastoma is thought to be maintained by a restricted population of cancer cells, stem-like cells that express CD133 transmembrane protein. Expression levels of CD133 gene has been linked to a poor prognostic molecular subgroup and is not overexpressed by the PDGF-driven proneural group. Thus, the significance of CD133+ cells for gliomagenesis of the proneural group is undetermined. In addition, the role of the CD133 protein remains elusive and controversial, which results from the difficult isolation of CD133+ cells that has largely relied on the use of antibodies to ill-defined glycosylated epitopes of CD133. Here, we used a knockin lacZ reporter mouse, Prom1lacZ/+, to track Prom1+ cells in the brain and found that Prom1 (prominin1, murine CD133 homologue) is expressed by cells that co-express markers characteristic of neuronal, glial and vascular lineage phenotype. In proneural tumors derived from injection of RCAS-PDGF into the brain of tv-a;Ink4a-Arf-/- Prom1lacZ/+ mice, Prom1+ cells co-express markers for astrocytes and endothelial cells. Therefore, we characterize the tumor propagation in a murine model and found that the mice co-transplanted with Prom1 endothelium and proneural tumor spheres cells had significant tumor burden and vascular proliferation (angiogenesis). Specific genes in Prom1 endothelium are identified that code for endothelial signaling modulators that most likely support proneural tumor progression and can be potential targets for anti-angiogenic therapy. Cells were sorted via FACS to obtain a population of CD31+CD133- cells and a population of CD31+CD133+ cells. Total RNA was extracted from each population and gene expression was assayed on Affymetrix Mouse 430 2.0 arrays with one array per cell population.
2013-12-31 | E-GEOD-43931 | biostudies-arrayexpress
Project description:The vast majority of cold sensitive DRG neurons from mice do not express the voltage-gated sodium channel NaV1.8. Therefore, we aimed to compare the molecular profiles of NaV1.8 and non-NaV1.8-expressing neurons using microarray analysis. Fluorescent activated cell sorting was performed at 4 degrees centigrade on acutely dissociated DRG neurons from mice expressing NaV1.8-Cre, Pirt-GCaMP3 and a Cre-dependent global reporter (td tomato). NaV1.8-expressing neurons were sorted based on their reporter fluorescence (td tomato; red) and putative cold sensing neurons were sorted based on their GCaMP3 fluorescence at 4 degrees centigrade and absence of Cre-dependent reporter fluorescence. A total of three mice were used (samples one, two and three) with GCaMP3 only and NaV1.8-expressing neurons forming two relative populations within each sample (eg. GC3 one is the experimental counterpart of Tom one).
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