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A genome-wide CRISPR activation screen identifies ETV7 as a negative regulator of the interferon response

ABSTRACT: A genome-wide CRISPR activation screen identifies ETV7 as a negative regulator of the interferon response

PROVIDER: PRJNA590656 | ENA |

REPOSITORIES: ENA

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ETV7 and interferon response

Project description:ETV7 and interferon response

| PRJNA590651 | ENA

A genome-wide CRISPR activation screen identifies ETV7 as a negative regulator of the interferon response

Project description:Identification of factors that negatively regulate the interferon response

2019-11-21 | GSE140717 | GEO

Impact of ETV7 activity on interferon-stimulated gene expression in 293T cells treated with interferon alpha

Project description:293T cells constitutively expressing ETV7 have reduced expression of interferon-stimulated genes.

2019-11-21 | GSE140709 | GEO

Deciphering the gene expression network regulated by ETV7

Project description:Cancer stem cells (CSCs) represent a population of cells within the tumor able to drive tumorigenesis and known to be highly resistant to conventional chemotherapy and radiotherapy. In this work, we show a new role for ETV7, a transcriptional repressor member of the ETS family, in promoting breast cancer stem-like cells plasticity and resistance to chemo- and radiotherapy in breast cancer (BC) cells. We observed that MCF7 and T47D BC-derived cells stably over-expressing ETV7 showed reduced sensitivity to the chemotherapeutic drug 5-Flouororuacil and to radiotherapy, accompanied by an adaptive proliferative behavior observed in different culture conditions. We further noticed that alteration of ETV7 expression could significantly affect the population of breast CSCs, measured by CD44+/CD24low cell population and mammosphere formation efficiency. By transcriptome profiling, we identified a signature of Interferon-responsive genes significantly repressed in cells over-expressing ETV7, which could be responsible for the increase in the breast CSCs population, as this could be partially reverted by the treatment with IFN-b. Lastly, we show that the expression of the IFN-responsive genes repressed by ETV7 could have prognostic value in breast cancer, as low expression of these genes was associated with a worse prognosis. Therefore, we propose a novel role for ETV7 in breast cancer stem cells’ plasticity and associated resistance to conventional chemotherapy and radiotherapy, which involves the repression of a group of IFN-responsive genes, potentially reversible upon IFN-b treatment. We, therefore, suggest that an in-depth investigation of this mechanism could lead to novel breast CSCs targeted therapies and to the improvement of combinatorial regimens, possibly involving the therapeutic use of IFN-b, with the aim of avoiding resistance development and relapse in breast cancer.

2021-07-28 | GSE152580 | GEO

CRISPR screen for interferon-alpha inducible inhibitors of yellow fever virus replication

Project description:Host cells produce interferon (IFN) in response to viral infections. Secreted interferon results in the transcription and production of hundreds of interferon-stimulated genes (ISGs). A genome-wide CRISPR screen using IFN alpha-treated Huh7.5 cells was performed to determine which ISGs were required in order for host cells to suppress yellow fever virus (YFV) infection.

2018-10-25 | GSE121710 | GEO

Impact of ETV7 activity on interferon-stimulated gene expression in 293T cells treated with interferon alpha

Project description:Impact of ETV7 activity on interferon-stimulated gene expression in 293T cells treated with interferon alpha

| PRJNA590633 | ENA

CRISPR screen for interferon-alpha inducible inhibitors of yellow fever virus replication

Project description:CRISPR screen for interferon-alpha inducible inhibitors of yellow fever virus replication

| PRJNA498126 | ENA

Haploid genome-wide screens for essential components and negative regulators of interferon lambda signaling in human cells

Project description:We undertook a unbiased genome-wide haploid genetic screen to identify new components in interferon lambda signaling. In addition, we performed a genome-wide screen to identify genes that repress spontaneous activation of interferon stimulated genes in the absence of interferon. Both of these screens were performed using a HAP1 cell line containing GFP reporter under the transcriptional regulation of the Interferon-Stimulated Response Element from IFIT2. We also overexpressed IL28RA (IFNLR1) in this cell line, in order to sensitize the cells to type III interferon

2017-07-25 | E-MTAB-5866 | biostudies-arrayexpress

A Virus-Packageable CRISPR Screen Identifies Host Factors Mediating Interferon Inhibition of HIV

Project description:Interferon (IFN) inhibits HIV replication by inducing an array of antiviral effectors. Here we describe a novel CRISPR knockout screening approach to identify the ensemble of these HIV restriction factors. We assembled a CRISPR sgRNA library specific for Interferon Stimulated Genes (ISGs) into a modified lentiviral vector that allows for packaging of sgRNA-encoding genomes in trans into budding HIV-1 particles. We observed that knockout of Zinc Antiviral Protein (ZAP) improved the performance of the screen due to ZAP-mediated inhibition of the vector. We identify a small panel of IFN-induced HIV restriction factors, including MxB, IFITM1, Tetherin/BST2 and TRIM5 which together explain the inhibitory effects of IFN on the HIV-1 LAI strain in THP-1 cells. Further, we identify novel HIV dependency factors, including SEC62 and TLR2. The ability of IFN-induced restriction factors to inhibit an HIV strain to replicate in human cells suggests that these human restriction factors are incompletely antagonized.

2018-08-17 | GSE118631 | GEO

A Virus-Packageable CRISPR Screen Identifies Host Factors Mediating Interferon Inhibition of HIV

Project description:A Virus-Packageable CRISPR Screen Identifies Host Factors Mediating Interferon Inhibition of HIV

| PRJNA486290 | ENA