Gene expression analysis of hematopoietic stem cells based on Syndecan-2 surface expression
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA637066 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11919054.fastq.gz | Fastqsanger.gz | |||
| SRR11919056.fastq.gz | Fastqsanger.gz | |||
| SRR11919057.fastq.gz | Fastqsanger.gz | |||
| SRR11919060.fastq.gz | Fastqsanger.gz | |||
| SRR11919061.fastq.gz | Fastqsanger.gz |
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Project description:Analysis of how Syndecan-2 expression identifies hematopoietic stem cells with unique gene expression profiles. We tested the hypothesis that Syndecan-2 expression enriches for hematopoietic stem cell gene expression programs. The results provide important insight into how Syndecan-2 can be used to isolate hematopoietic stem cells with distinct hematopoietic properties.
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Project description:To dissect the functions of syndecan-1 in the nucleus, and separate them from functions related to the cell-surface, we transfected fibrosarcoma cells with two constructs: one encoding the full-length syndecan-1, which translocates to the nucleus and another encoding syndecan-1 lacking the RMKKK nuclear localization signal with hampered nuclear translocation. Using this model system, we combined global transcriptomic and proteomic approaches in order to disclose the molecular mechanisms governing the nuclear translocation and its related functions. Our analysis identified several genes and pathways related to the nuclear compartment TGF-β pathway was activated by nuclear syndecan-1 and three genes were significantly altered by NLS deletion: NEK11 , DOCK8 , and EGR-1 as potential candidates coupled to syndecan-1 in the nucleus.
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Project description:We evaluated the effect of syndecan-1 in various cell-based and animal models of lung cancer and found that lung tumorigenesis was promoted when cells lose syndecan-1 expression. We also demonstrate that syndecan-1 (or lack thereof) alters the microRNA (miRNA) cargo carried within exosomes exported from lung cancer cells. Analysis of the changes in miRNA expression identifies a distinct shift toward augmented pro-cancerous signaling, which are consistent with the changes found in lung adenocarcinoma. In all, our work identifies syndecan-1 as an important factor on lung cancer cells that control its ability to shape the lung tumor microenvironment through alterations in miRNA packaging within exosomes.
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Project description:We evaluated the effect of syndecan-1 in various cell-based and animal models of lung cancer and found that lung tumorigenesis was promoted when cells lose syndecan-1 expression. We also demonstrate that syndecan-1 (or lack thereof) alters the microRNA (miRNA) cargo carried within exosomes exported from lung cancer cells. Analysis of the changes in miRNA expression identifies a distinct shift toward augmented pro-cancerous signaling, which are consistent with the changes found in lung adenocarcinoma. In all, our work identifies syndecan-1 as an important factor on lung cancer cells that control its ability to shape the lung tumor microenvironment through alterations in miRNA packaging within exosomes.
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Project description:Syndecan-2 was found to act as a tumor suppressor in osteosarcoma and to mediate the apoptotic response to cytotoxic agents. To determine new mechanisms that control cell survival and apoptosis in osteosarcoma cells, we aim to show target genes that are involved downstream of this proteoglycan during apoptosis induction. We aim to compare the modifications induced by syndecan-2 overexpression in two different human osteosarcoma cell lines using a lentiviral vector coding the human syndecan-2. Syndecan-2 lentiviral vector (SY) and control empty lentiviral vector (VV) were transducted in two different human osteosarcoma cell lines in a dye-swap experiment.
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Project description:Syndecan-2 was found to act as a tumor suppressor in osteosarcoma and to mediate the apoptotic response to cytotoxic agents. To determine new mechanisms that control cell survival and apoptosis in osteosarcoma cells, we aim to show target genes that are involved downstream of this proteoglycan during apoptosis induction. We aim to compare the modifications induced by syndecan-2 overexpression in two different human osteosarcoma cell lines using a lentiviral vector coding the human syndecan-2.
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Project description:We aimed to investigate the function of syndecan-1 in tumor cell adhesion and migration, with special focus on the importance of its distinct protein domains, to better understand the structure-function relationship of syndecan-1 in tumor progression. We utilized two mesenchymal tumor cell lines which were transfected to stably overexpress full-length syndecan-1 or truncated variants: the 78 which lacks the extracellular domain except the DRKE sequence proposed to be essential for oligomerization, the 77 which lacks the whole extracellular domain, and the RMKKK which serves as a nuclear localization signal. Various bioassays for cell adhesion, chemotaxis, random movement and wound healing were studied. Furthermore we performed gene microarray to analyze the global gene expression pattern influenced by syndecan-1. We found that full-length syndecan-1 enhanced cell adhesion in a dose-dependent manner. The truncated constructs only affected adhesion marginally, or not at all. Both full-length syndecan-1 and all its distinct domains inhibited serum-induced cell migration and wound closure. The full-length syndecan-1 and the 78 constructs specifically reduced cell motility/migration in random movement assay. Cell adhesion depends on the extracellular domain and also associates with the DRKE motif. Effects of syndecan-1 on migration are more complex; the pro-adhesive effect of the extracellular domain is one factor hampering migration, but the transmembrane/cytoplasmic portion seems to have additional impact. Gene microarray analysis showed that a number of genes involved in cell adhesion and migration were differentially expressed in syndecan-1 overexpressing cells. Our results demonstrate that syndecan-1 regulates mesenchymal tumor cell adhesion and migration, and different domains have differential effects. Our study provides new inputs into the better understanding of structure-function relationship of this PG in tumor progression. Gene expression profiles (Human Gene 1.0 ST) of malignant mesothelioma cells were studied in syndecan-1 overexpressing cells (N=3) and vector control cells (N=3) .
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Project description:The transcriptomic responses of syndecan-1 silencing in a human mesothelioma cell line was followed with microarray analysis. To project the transcriptome analysis on the full-dimensional picture of cellular regulation, we applied a novel method of network enrichment analysis which elucidated signalling relations between differentially expressed genes and pathways acting via various molecular mechanisms. Our results suggest that syndecan-1 regulates cell proliferation in a highly complex way, although the exact contribution of the altered pathways necessitates further functional studies. Gene expression profiles (Human Gene 1.0 ST) of malignant mesothelioma cells were studied in cells silenced for syndecan-1 (N=3) and scrambled control cells (N=3)
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Project description:We aimed to investigate the function of syndecan-1 in tumor cell adhesion and migration, with special focus on the importance of its distinct protein domains, to better understand the structure-function relationship of syndecan-1 in tumor progression. We utilized two mesenchymal tumor cell lines which were transfected to stably overexpress full-length syndecan-1 or truncated variants: the 78 which lacks the extracellular domain except the DRKE sequence proposed to be essential for oligomerization, the 77 which lacks the whole extracellular domain, and the RMKKK which serves as a nuclear localization signal. Various bioassays for cell adhesion, chemotaxis, random movement and wound healing were studied. Furthermore we performed gene microarray to analyze the global gene expression pattern influenced by syndecan-1. We found that full-length syndecan-1 enhanced cell adhesion in a dose-dependent manner. The truncated constructs only affected adhesion marginally, or not at all. Both full-length syndecan-1 and all its distinct domains inhibited serum-induced cell migration and wound closure. The full-length syndecan-1 and the 78 constructs specifically reduced cell motility/migration in random movement assay. Cell adhesion depends on the extracellular domain and also associates with the DRKE motif. Effects of syndecan-1 on migration are more complex; the pro-adhesive effect of the extracellular domain is one factor hampering migration, but the transmembrane/cytoplasmic portion seems to have additional impact. Gene microarray analysis showed that a number of genes involved in cell adhesion and migration were differentially expressed in syndecan-1 overexpressing cells. Our results demonstrate that syndecan-1 regulates mesenchymal tumor cell adhesion and migration, and different domains have differential effects. Our study provides new inputs into the better understanding of structure-function relationship of this PG in tumor progression.
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Project description:Biomechanical stimuli and extracellular matrix cues are important initiators for the cardiac remodeling process, and signaling hubs in the sarcolemma are important contact points between the extracellular space and cell interior, sensing and transducing biomechanical signals into a cellular response. The transmembrane proteoglycan syndecan-4 localizes to these attachment points and has been shown important in initial stages of cardiac remodeling. The objective of this study was to map the cardiac interactome of syndecan-4 to better understand its function and downstream signaling mechanisms. By combining two different affinity purification methods with mass spectrometry, we identified the cardiac syndecan-4 interactome to consist of 21 novel and 31 previously described interaction partners. 12of the novel partners were further validated to bind syndecan-4 in HEK293 (MPP7, PARVB, CCT5, CDK9, EIF22S1, PFKM, RASIP, EIF4B, PTRF/CAVIN1, AP3D1, EPB4.1 and MLP/CSRP3). 19 of the interactome partners bound differently to syndecan-4 in left ventricle lysate from aorta banded hypertrophic failing (ABHF) rats. One of these partners was the well-known mechanotransducer MLP, which showed a direct and significant increased binding to syndecan-4 in ABHF. Nuclear translocation is important in MLP mediated signalling and we found less MLP in nuclear enriched fractions from syndecan-4-/- mouse left ventricles, but an increase in nuclear MLP when syndecan-4 was overexpressed in a cardiomyocyte cell line. In the presence of a cell-permeable syndecan-4-MLP disruptor peptide, the nuclear MLP level was significantly reduced. This suggests syndecan-4 to be a mediator of nuclear translocation of MLP in the heart.
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