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CRISPR-SaCas9-KKH targeting of miR-21 through a single adeno-associated virus vector prolongs survival of GB-bearing mice

ABSTRACT: CRISPR-SaCas9-KKH targeting of miR-21 through a single adeno-associated virus vector prolongs survival of GB-bearing mice

PROVIDER: PRJNA1161642 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30676000_1.fastq.gz	Fastqsanger.gz
	SRR30676000_2.fastq.gz	Fastqsanger.gz
	SRR30676001_1.fastq.gz	Fastqsanger.gz
	SRR30676001_2.fastq.gz	Fastqsanger.gz
	SRR30676002_1.fastq.gz	Fastqsanger.gz

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CRISPR-SaCas9-KKH targeting of miR-21 through a single adeno-associated virus vector prolongs survival of GB-bearing mice

Project description:Glioblastoma (GB), the most aggressive tumor of the central nervous system (CNS), has poor patient outcomes with limited effective treatments available. MicroRNA-21 (miR-21) is a known oncogene, abundantly expressed in many cancer types. MiR-21 promotes glioblastoma progression, and lack of miR-21 reduces tumorigenic potential of tumor. Here, we propose a single adeno-associated virus (AAV) vector strategy targeting miR-21 using the Staphylococcus aureus Cas9 ortholog (SaCas9) guided by a single-guide RNA (sgRNA). Our results demonstrate that AAV8 is a well-suited AAV serotype to express SaCas9-KKH/sgRNA at the tumor site in an orthotopic glioblastoma model. The SaCas9-KKH induced a genomic deletion, resulting in lowered miR-21 levels in the brain, leading to reduced tumor growth and improved overall survival. In this study we demonstrated that a single AAV-mediated mir-21 disruption influences glioma development resulting in beneficial anti-tumor outcomes in GB-bearing mice.

2024-11-27 | GSE277282 | GEO

adeno-associated virus

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Small RNA deep sequencing of HEK 293T cells treated with an Adeno vector encoding the Vaccinia virus VP55 protein

Project description:To assess the efficacy of AdV-VP55 mediated degredation of host miRNAs. Small RNA profiles of HEK 293T cells treated with type 5 Adeno vectors expressing either GFP or GFP-VP55 for 24 hours

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Epigenetic Targeting of Bromodomain Protein BRD4 Counteracts Cancer Cachexia and Prolongs Survival

Project description:Cancer cachexia is a devastating metabolic syndrome characterized by systemic inflammation and massive muscle and adipose tissue wasting. Although cancer cachexia is responsible for approximately one third of cancer deaths, no effective therapies are available and the underlying mechanisms have not been fully elucidated.We have found that (+)-JQ1 administration protects tumor-bearing mice from body weight loss, muscle and adipose tissue wasting. Remarkably, in C26-tumor bearing mice (+)-JQ1 administration dramatically prolongs survival, without directly affecting tumor growth. By ChIP-seq analyses, we unveil that the BET proteins directly promote the muscle atrophy program during cachexia. Consistently, BET pharmacological blockade prevents the activation of catabolic genes associated with skeletal muscle atrophy and decreases IL6 systemic levels. Overall, these findings indicate that BET may represent a promising therapeutic target in the management of cancer cachexia.

2017-10-01 | GSE104155 | GEO

adeno-associated virus 8

Project description:adeno-associated virus 8 Raw sequence reads

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Lactiplantibacillus plantarum strain:GB-LP1

Project description:Genome analysis of Lactobacillus plantarum GB-LP1

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Gymnopus earleae strain:GB-263.02

Project description:Gymnopus earleae GB-263.02 Transcriptome - RNA-Gymae

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Transcription profiling of human brain neuronal (SH-SY5Y) cell lines exposed to sarin (GB)

Project description:Total RNA was isolated from sarin (GB) treated (n = 6 flasks) untreated (control n = 6) neuronal (SH-SY5Y) cell lines using RNeasyÂ® mini kit. The preparation and processing of labeled, fragmented cRNA for hybridization has been performed according to the manufacturerâs protocols (Affymetrix, Santa Clara, CA). (Biological Replicates for each time points). Experiment Overall Design: Global gene expression pattern of human neuronal (SH-SY5Y) cell lines exposed to sarin (GB) at various time points.

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Gene transfer of heme oxygenase-1 using an adeno-associated virus serotype 6 vector prolongs cardiac allograft survival.

Project description:Introduction. Allograft survival can be prolonged by overexpression of cytoprotective genes such as heme oxygenase-1 (HO-1). Modifications in vector design and delivery have provided new opportunities to safely and effectively administer HO-1 into the heart prior to transplantation to improve long-term graft outcome. Methods. HO-1 was delivered to the donor heart using an adeno-associated virus vector (AAV) with a pseudotype 6 capsid and vascular endothelial growth factor (VEGF) to enhance myocardial tropism and microvascular permeability. Survival of mouse cardiac allografts, fully or partially mismatched at the MHC, was determined with and without cyclosporine A. Intragraft cytokine gene expression was examined by PCR. Results. The use of AAV6 to deliver HO-1 to the donor heart, combined with immunosuppression, prolonged allograft survival by 55.3% when donor and recipient were completely mismatched at the MHC and by 94.6% if partially mismatched. The combination of gene therapy and immunosuppression was more beneficial than treatment with either AAV6-HO-1 or CsA alone. IL-17a, b, e and f were induced in the heart at rejection. Conclusions. Pretreatment of cardiac allografts with AAV6-HO-1 plus cyclosporine A prolonged graft survival. HO-1 gene therapy represents a beneficial adjunct to immunosuppressive therapy in cardiac transplantation.

| S-EPMC3480008 | biostudies-literature

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