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Expression data from DEGs in human ESCC EC109 cells transfected with empty lentiviral vector (Lv-NC) or lentiviral vector carrying carrying KDM5C specific shRNA (Lv-shKDM5C)

ABSTRACT: Expression data from DEGs in human ESCC EC109 cells transfected with empty lentiviral vector (Lv-NC) or lentiviral vector carrying carrying KDM5C specific shRNA (Lv-shKDM5C)

PROVIDER: PRJNA667699 | ENA |

REPOSITORIES: ENA

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Expression data from DEGs in human ESCC EC109 cells transfected with empty lentiviral vector (Lv-NC) or lentiviral vector carrying carrying KDM5C specific shRNA (Lv-shKDM5C)

Project description:Expression data from different expressed genes (DEGs) in human esophageal squamous cell carcinoma (ESCC) EC109 cells transfected with empty lentiviral vector (Lv-NC) or lentiviral vector carrying carrying KDM5C specific shRNA (Lv-shKDM5C) Lysine demethylase 5C (KDM5C), a member of lncRNAs, has tumor-suppressor properties and is downregulated in the majority of malignancies. KDM5C was found to suppress some sorts of tumors through regulating epithelial mesenchymal transformation,inducing cell cycle arrest,triggering apoptosis and so on. We used microarrays to investigate the possible regulatory mechanism of KDM5C in ESCC cell line.

2021-10-06 | GSE159102 | GEO

Expression data from different expressed genes(DEGs) in human esophageal squamous cell carcinoma(ESCC) EC109 cells transfected with empty lentiviral vector(Lv-NC) or lentiviral vector carrying MEG3(Lv-MEG3)

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Expression data from nucleus accumbens of rats infused with lentivirus LV-GFP and LV-miR-495 overexpression constructs

Project description:The goal of the study was to determine the effect of lentiviral- mediated overexpression of miR-495 (LV-miR-495) on the levels of gene expression in the nuclues accumbens of rats relative to control rats injected with the empty vector (LV-GFP). We used Rat Gene 2.0 ST Affymetrix expression arrays ( to identify genes whose expression levels were downregulated by overexpression of miR-495.

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β-Globin Lentiviral Vectors Have Reduced Titers Due to Incomplete Vector RNA Genomes and Lowered Virion Production

Project description:Lentiviral vectors (LV) commonly used for the treatment of hemoglobinopathies often have low titers and sub-optimal gene transfer efficiency for human hematopoietic stem and progenitor cells (HSPC), hindering clinical translation and commercialization for ex vivo gene therapy. We observed that a high percentage of β-globin LV viral genomic RNAs were incomplete towards the 3’ end in packaging cells and in released vector particles. The incomplete vector genomes impeded reverse transcription in target cells, limiting stable gene transfer to HSPC. By combining three modifications to vector design and production (shortening the vector length to 5.3-kb; expressing TAT protein during packaging; and packaging in PKR-/- cells) there was a 30-fold increase in vector titer and a 3-fold increase in vector infectivity in HSPC. These approaches may improve the manufacturing of β-globin and other complex LVs for enhanced gene delivery and may facilitate clinical applications.

2020-09-21 | GSE158252 | GEO

Project description:Maternally expressed gene 3 (MEG3), a member of lncRNAs, has tumor-suppressor properties and is downregulated in the majority of malignancies. MEG3 was found to suppress some sorts of tumors through regulating epithelial mesenchymal transformation,inducing cell cycle arrest,triggering apoptosis and so on. We used microarrays to investigate the possible regulatory mechanism of MEG3 in ESCC cell line.

2020-10-20 | GSE142036 | GEO

Partial correction of immunodeficiency by lentiviral vector gene therapy in mouse models carrying Rag1 hypomorphic mutations

Project description:Partial correction of immunodeficiency by lentiviral vector gene therapy in mouse models carrying Rag1 hypomorphic mutations

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Integrome signatures of lentiviral gene therapy for SCID-X1 patients

Project description:Lentiviral vector (LV)-based gene therapy holds promise for a broad range of diseases. Analyzing more than 280,000 vector integration sites (VISs) in 273 samples from 10 patients with X-linked severe combined immunodeficiency (SCID-X1), we discovered shared LV integrome signatures in 9 out of 10 patients in relation to the genomics, epigenomics, and 3D structure of the human genome. VISs were enriched in the nuclear sub-compartment A1 and integrated into super-enhancers close to nuclear pore complexes. These signatures were validated in T cells transduced with an LV encoding a CD19-specific chimeric antigen receptor. Intriguingly, the one patient whose VISs deviated from the identified integrome signatures had a distinct clinical course. Comparison of LV and gamma retrovirus integromes regarding their 3D genome signatures, identified differences that might explain the lower risk of insertional mutagenesis in LV-based gene therapy. Our findings suggest that LV integrome signatures, shaped by common features such as genome organization, may impact the efficacy of LV-based cellular therapies.

2023-10-06 | GSE163082 | GEO

Integrome signatures of lentiviral gene therapy for SCID-X1 patients

2023-10-06 | GSE163081 | GEO

Super-enhancer based development of an endothelial specific lentiviral vector

Project description:Hypoxia-regulated endothelial-specific lentiviral vector that can be used for endothelial-targeted gene therapy.

2021-08-12 | GSE151832 | GEO

Lentiviral Vectors Escape Innate Sensing but Trigger p53 In Human Hematopoietic Stem Cells

Project description:In the context of lentiviral vector (LV)-mediated gene correction of hematopoietic stem and progenitor cells (HSPC), the viral origin of LV could trigger cellular responses with potential functional consequences that have not been investigated to date. Here, a time-course genome-wide transcriptional profiling of transduced human HSPC reveals a remarkably limited impact of LV on cellular gene expression, supporting some stealth features of the vector. In particular, LV efficiently escaped innate immune sensing that instead led to robust type I IFN signaling upon transduction with a gamma-retroviral vector. However, recognition of LV DNA prior to integration did trigger DNA damage responses that were activated also by non-integrating Adeno-associated vector DNA. As a consequence of this transient p53 activation, transduced HSPC showed increased apoptosis in vitro and reduced engraftment in vivo at limiting cell doses, but no long-term impact or competitive disadvantage were detected. Pharmacological inhibition of the LV signaling partially rescued both apoptosis and engraftment, potentially providing a novel strategy to further dampen the impact of ex vivo gene therapy on HSPC. Overall, our results shed light on the molecular mechanisms of viral vector sensing in HSPC and provide critical insight for the development of more stealth gene therapy strategies.

2017-06-28 | GSE92652 | GEO

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