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Syndecan-1 controls lung tumorigenesis by regulating microRNAs packaged in exosomes [A549]

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE106277 | GEO | 2017/10/28

SECONDARY ACCESSION(S): PRJNA416109

REPOSITORIES: GEO

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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

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

Project description:Syndecan-1 controls lung tumorigenesis by regulating microRNAs packaged in exosomes

| PRJNA416251 | ENA

Syndecan-1 controls lung tumorigenesis by regulating microRNAs packaged in exosomes [A549]

Project description:Syndecan-1 controls lung tumorigenesis by regulating microRNAs packaged in exosomes [A549]

| PRJNA416109 | ENA

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

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

| PRJNA416253 | ENA

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-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

Syndecan-2 and apoptosis in osteosarcoma

2013-09-23 | GSE19913 | GEO

Syndecan-1 promotes lung fibrosis by regulating epithelial reprogramming through extracellular vesicles (RNA-Seq)

Project description:We evaluted the effects of extracellular vesicles of bleomycin-injured wild-type and syndecan-1 deficient mice on mouse lung epithelial cell line (MLE-12) total transcriptomic changes (bulk mRNA sequencing)

2019-07-24 | GSE134741 | GEO

Syndecan liver cancer nanoHPLC-MS/MS results

Project description:Liver cancer was induced in mouse model organisms with diethylnitrosamine. It was found the the introduction of human Syndecan significantly slowed down the carcinogenesis. The proteomic profile of the syndecan treated livers proved to be significantly different from the non-treated samples. Details are shown in the paper.

2021-01-09 | MSV000086679 | MassIVE

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

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