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Modulation of Syndecan-1/4 reduces the invasive potential of endometrioma through TGF-β signalling

ABSTRACT: Modulation of Syndecan-1/4 reduces the invasive potential of endometrioma through TGF-β signalling

PROVIDER: PRJNA557473 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9861820.fastq.gz	Fastqsanger.gz
	SRR9861830.fastq.gz	Fastqsanger.gz
	SRR9861840.fastq.gz	Fastqsanger.gz
	SRR9861850.fastq.gz	Fastqsanger.gz
	SRR9861821.fastq.gz	Fastqsanger.gz

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Modulation of Syndecan-1/4 reduces the invasive potential of endometrioma through TGF-β signalling

Project description:We report that modulation of high SDC -1/-4 within certain endometriomas in women having ovarian endometriosis, reversed its higher invasion potential and downregulated several molecules incolved in cancer development.

2020-10-06 | GSE135122 | GEO

Expression data generated by syndecan-1 silencing in malignant mesothelioma STAV-AB cell line

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)

2012-11-01 | E-GEOD-37843 | biostudies-arrayexpress

Expression data generated by full-length and truncated syndecan-1 overexpression in B6FS fibrosarcoma cell line

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.

2017-09-10 | GSE81504 | GEO

The cardiac syndecan-4 interactome:A role for syndecan-4 innuclear translocation of muscle LIM protein (MLP)

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.

2019-04-09 | PXD011249 | Pride

Syndecan-2 and apoptosis in osteosarcoma

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.

2013-09-23 | E-GEOD-19913 | biostudies-arrayexpress

Expression data generated by syndecan-1 silencing in malignant mesothelioma STAV-AB cell line

2012-11-01 | GSE37843 | GEO

Syndecan-2 and apoptosis in osteosarcoma

2013-09-23 | GSE19913 | GEO

TGF-beta signalling through SMAD1/5 is required for epithelial-to-mesenchymal transition

Project description:TGF-beta treatment leads to SMAD1/5 phosphorylation. However, the ability of SMAD1/5 to bind chromatin downstream of TGF-beta signalling is unknown. We performed ChIP-sequencing for pSMAD1/5 and SMAD3 to identify binding sites for pSMAD1/5 upon TGF-beta stimulation and identified preferential pSMAD1/5 binding at SMAD1/5:SMAD4 consensus sites.

2018-02-16 | GSE92443 | GEO

Gene expression analysis of hematopoietic stem cells based on Syndecan-2 surface expression

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.

2022-03-09 | GSE151733 | GEO

Syndecan-1 controls lung tumorigenesis by regulating microRNAs packaged in exosomes [EKVX]

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.

2017-10-30 | GSE106303 | GEO

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