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Dual targeted extracellular vesicles regulating oncogenic genes in pancreatic cancer [sRNAseq]

ABSTRACT: Dual targeted extracellular vesicles regulating oncogenic genes in pancreatic cancer [sRNAseq]

PROVIDER: PRJNA925924 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23170569.fastq.gz	Fastqsanger.gz
	SRR23170570.fastq.gz	Fastqsanger.gz
	SRR23170571.fastq.gz	Fastqsanger.gz
	SRR23170572.fastq.gz	Fastqsanger.gz
	SRR23170573.fastq.gz	Fastqsanger.gz

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Dual targeted extracellular vesicles regulating oncogenic genes in pancreatic cancer [sRNAseq]

Project description:Pancreatic ductal adenocarcinoma (PDAC) tumors carry multiple gene mutations and respond poorly to treatments. There is currently an unmet need for drug carriers that can deliver multiple gene cargoes to high solid tumor burden like PDAC. Here, we report a dual-targeted extracellular vesicle (EV) carrying high loads of RNA that effectively suppresses large PDAC tumors in mice. The EV surface contains a CD64 protein that has a tissue targeting peptide and a humanized monoclonal antibody. Cells sequentially transfected with plasmid DNAs encoding for the RNA and protein of interest by Transwell®-based asymmetric cell electroporation released abundant targeted EVs with high RNA loading. Together with a low dose chemotherapy drug, Gemcitabine, dual-targeted EVs effectively suppressed large orthotopic PANC-1 and patient derived xenograft tumors in mice and extended animal survival. This work presents a clinically accessible and scalable way to produce abundant EVs for delivering multiple gene cargoes to large solid tumors.

2023-10-02 | GSE223397 | GEO

Dual targeted extracellular vesicles regulating oncogenic genes in pancreatic cancer

Project description:Dual targeted extracellular vesicles regulating oncogenic genes in pancreatic cancer

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Dual targeted extracellular vesicles regulating oncogenic genes in pancreatic cancer [Human Array]

Project description:Dual targeted extracellular vesicles regulating oncogenic genes in pancreatic cancer [Human Array]

| PRJNA925941 | ENA

Dual targeted extracellular vesicles regulating oncogenic genes in pancreatic cancer [Mouse Array]

Project description:Dual targeted extracellular vesicles regulating oncogenic genes in pancreatic cancer [Mouse Array]

| PRJNA925942 | ENA

Dual targeted extracellular vesicles regulating oncogenic genes in pancreatic cancer [Mouse Array]

Project description:Pancreatic ductal adenocarcinoma (PDAC) tumours carry multiple gene mutations and respond poorly to treatments. There is currently an unmet need for drug carriers that can deliver multiple gene cargoes to high solid tumour burden like PDAC. Here, we report a dual-targeted extracellular vesicle (EV) carrying high loads of RNA that effectively suppresses large PDAC tumours in mice. The EV surface contains a CD64 protein that has a tissue targeting peptide and a humanized monoclonal antibody. Cells sequentially transfected with plasmid DNAs encoding for the RNA and protein of interest by Transwell®-based asymmetric cell electroporation released abundant targeted EVs with high RNA loading. Together with a low dose chemotherapy drug, Gemcitabine, dual-targeted EVs effectively suppressed large orthotopic PANC-1 and patient derived xenograft tumours in mice and extended animal survival. This work presents a clinically accessible and scalable way to produce abundant EVs for delivering multiple gene cargoes to large solid tumours.

2023-10-02 | GSE223408 | GEO

Dual targeted extracellular vesicles regulating oncogenic genes in pancreatic cancer [Human Array]

2023-10-02 | GSE223407 | GEO

Dual targeted extracellular vesicles regulating oncogenic genes in pancreatic cancer

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

2023-10-01 | GSE223409 | GEO

Dual targeted extracellular vesicles regulate oncogenic genes in advanced pancreatic cancer.

Project description:Pancreatic ductal adenocarcinoma (PDAC) tumours carry multiple gene mutations and respond poorly to treatments. There is currently an unmet need for drug carriers that can deliver multiple gene cargoes to target high solid tumour burden like PDAC. Here, we report a dual targeted extracellular vesicle (dtEV) carrying high loads of therapeutic RNA that effectively suppresses large PDAC tumours in mice. The EV surface contains a CD64 protein that has a tissue targeting peptide and a humanized monoclonal antibody. Cells sequentially transfected with plasmid DNAs encoding for the RNA and protein of interest by Transwell®-based asymmetric cell electroporation release abundant targeted EVs with high RNA loading. Together with a low dose chemotherapy drug, Gemcitabine, dtEVs suppress large orthotopic PANC-1 and patient derived xenograft tumours and metastasis in mice and extended animal survival. Our work presents a clinically accessible and scalable way to produce abundant EVs for delivering multiple gene cargoes to large solid tumours.

| S-EPMC10593751 | biostudies-literature

sRNAseq of Magnaporthe oryzae - Brachypodium distachyon pathosystems

Project description:sRNAseq of Magnaporthe oryzae - Brachypodium distachyon pathosystems

| PRJEB42392 | ENA

Dual regulation of Fbw7 function and oncogenic transformation by Usp28

Project description:Fbw7, the substrate recognition subunit of SCF(Fbw7) ubiquitin ligase, mediates turnover of multiple proto-oncoproteins and promotes its own degradation. Fbw7-mediated substrate degradation is antagonized by the Usp28 deubiquitinase. We now show, using knockout mice, that Usp28 preferentially deubiquitinates and stabilizes Fbw7. Monoallelic deletion of Usp28 maintains stable Fbw7 but destabilizes Fbw7 substrates. In contrast, complete knockout of Usp28 promotes Pin1-dependent autocatalytic turnover of Fbw7, accumulation of Fbw7 substrates and oncogenic transformation. Overexpression of Usp28 stabilizes both Fbw7 and its substrates and similarly enhances transformation. We propose that dual regulation of Fbw7 activity by Usp28 maintains physiological levels of Fbw7 substrates, and that both loss and overexpression of Usp28 in human cancer promote Fbw7 substrate accumulation. RNAseq experiments of E13.5 murine embryonic fibroblasts (MEFs) derived from animals in which Usp28 was either deleted (-/-), wildtype (+/+) or heterozygous (+/-). In a first set of experiments immortalized MEFs of all three genotypes were analysed in biological triplicates. In a second set of experiments immortalized and Ras transformed MEFs of all three genotypes and MEFs which overexpress USP28 (+/+/+) where sequenced in duplicates.

2015-05-01 | E-GEOD-59354 | biostudies-arrayexpress

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