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

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

PROVIDER: PRJNA416251 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6230320.fastq.gz	Fastqsanger.gz
	SRR6233840.fastq.gz	Fastqsanger.gz
	SRR6230321.fastq.gz	Fastqsanger.gz
	SRR6233841.fastq.gz	Fastqsanger.gz
	SRR6230322.fastq.gz	Fastqsanger.gz

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

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.

2017-10-28 | GSE106277 | GEO

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

2017-10-30 | GSE106303 | GEO

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

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]

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

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-10-30 | GSE106304 | GEO

Syndecan-1 Controls Lung Tumorigenesis by Regulating miRNAs Packaged in Exosomes.

Project description:Syndecan-1 is a transmembrane proteoglycan expressed prominently by lung epithelium and has pleiotropic functions such as regulating cell migration, proliferation, and survival. Loss of syndecan-1 expression by lung cancer cells is associated with higher-grade cancers and worse clinical prognosis. We evaluated the effects of syndecan-1 in various cell-based and animal models of lung cancer and found that lung tumorigenesis was moderated by syndecan-1. We also demonstrate that syndecan-1 (or lack thereof) alters the miRNA cargo carried within exosomes exported from lung cancer cells. Analysis of the changes in miRNA expression identified a distinct shift toward augmented procancer signaling consistent with the changes found in lung adenocarcinoma. Collectively, our work identifies syndecan-1 as an important factor in lung cancer cells that shapes the tumor microenvironment through alterations in miRNA packaging within exosomes.

| S-EPMC5963476 | biostudies-literature

Project description:Breast milk is a complex liquid that enriched in immunological components and affect the development of the infant immune system. Exosomes, the membranous vesicles of endocytic origin, are ubiquitously in various body fluids which can mediate intercellular communication. MicroRNAs (miRNAs), a well-defined group of non-coding small RNAs, in human breast milk are packaged inside exosomes. Here, we present the identification of miRNAs in human breast milk exosomes using deep sequencing technology. We found that the immune-related miRNAs are enriched in breast milk exosomes, and are resistant to the general harsh conditions. Four small RNA libraries in human breast milk exosomes from four healthy women (30 +/- 0.9 years old, primiparity) when the infant were aged at 60 days were sequenced.

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Exosomes packaged chromatin with dynamic H3R26me2s modification prevents cellular inflammation by blocking the cGAS-STING pathway [RNA-seq]

Project description:Exosomes DNA derived from genomic and mitochondrial could modulate type I IFN expression by triggering the cGAS-STING pathway. However, the chromatin modification of secreted exosomes involved in this process is largely unknown. Here, we could detect the histone H3R26me and H3K27ac in the components of secreted exosomes, meanwhile, a global decrease of H3R26 symmetric dimethylation (H3R26me2s) accompanied by the lowering enrichment of H3K27ac, and this distribution pattern was able to be verified by decreased H3R26me2s leading to the reduction of H3K27ac. Furthermore, these fragmented chromatins trans-located into cytoplasmic could repress cGAS-STING induction of IFNβ1 expression, which is further packaged into the exosomes. Collectively, our findings elucidate a novel pathway that which cells can actively transport the chromatin fragments of altered histone arginine methylation to alleviate the stimulation by damaged DNA. We perform RNA-seq to analysis the changes of gene expression in cells treated with bleomycin.

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Exosomes packaged chromatin with dynamic H3R26me2s modification prevents cellular inflammation by blocking the cGAS-STING pathway [CUT&Tag-seq]

Project description:Exosomes DNA derived from genomic and mitochondrial could modulate type I IFN expression by triggering the cGAS-STING pathway. However, the chromatin modification of secreted exosomes involved in this process is largely unknown. Here, we could detect the histone H3R26me and H3K27ac in the components of secreted exosomes, meanwhile, a global decrease of H3R26 symmetric dimethylation (H3R26me2s) accompanied by the lowering enrichment of H3K27ac, and this distribution pattern was able to be verified by decreased H3R26me2s leading to the reduction of H3K27ac. Furthermore, these fragmented chromatins trans-located into cytoplasmic could repress cGAS-STING induction of IFNβ1 expression, which is further packaged into the exosomes. Collectively, our findings elucidate a novel pathway that which cells can actively transport the chromatin fragments of altered histone arginine methylation to alleviate the stimulation by damaged DNA. We perform ChIP-seq to analysis the changes of histone modification in cells treated with bleomycin.

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