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In vivo CRISPR/Cas9 screen to identify candidate therapeutic gene targets to enhance docetaxel efficacy in prostate cancer

ABSTRACT: In vivo CRISPR/Cas9 screen to identify candidate therapeutic gene targets to enhance docetaxel efficacy in prostate cancer

PROVIDER: PRJEB40035 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR4508050.fastq.gz	Fastqsanger.gz
	ERR4508060.fastq.gz	Fastqsanger.gz
	ERR4508051.fastq.gz	Fastqsanger.gz
	ERR4508061.fastq.gz	Fastqsanger.gz
	ERR4508052.fastq.gz	Fastqsanger.gz

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In vivo CRISPR/Cas9 screen to identify candidate therapeutic gene targets to enhance docetaxel efficacy in prostate cancer

Project description:Docetaxel chemotherapy in metastatic prostate cancer offers only a modest survival benefit due to emerging resistance. To identify candidate therapeutic gene targets, we applied a murine prostate cancer orthograft model that recapitulates clinical invasive prostate cancer in a genome-wide CRISPR/Cas9 screen under docetaxel treatment pressure.

2020-10-07 | E-MTAB-9482 | biostudies-arrayexpress

RNA-seq analysis of TCEAL1 knock down with/without docetaxel treatment to enhance docetaxel efficacy in prostate cancer

Project description:Docetaxel chemotherapy in metastatic prostate cancer offers only a modest survival benefit due to emerging resistance. This experiment studies effect of TCEAL1 gene knock down with/without docetaxel treatment. The TCEAL1 gene was identified as the top candidate gene in vivo CRISPR/Cas9 screen.

2020-10-07 | E-MTAB-9484 | biostudies-arrayexpress

RNA-seq analysis of TCEAL1 knock down with/without docetaxel treatment to enhance docetaxel efficacy in prostate cancer

Project description:RNA-seq analysis of TCEAL1 knock down with/without docetaxel treatment to enhance docetaxel efficacy in prostate cancer

| PRJEB40036 | ENA

In vivo CRISPR/Cas9 knockout screen: TCEAL1 silencing enhances docetaxel efficacy in prostate cancer.

Project description:Docetaxel chemotherapy in metastatic prostate cancer offers only a modest survival benefit because of emerging resistance. To identify candidate therapeutic gene targets, we applied a murine prostate cancer orthograft model that recapitulates clinical invasive prostate cancer in a genome-wide CRISPR/Cas9 screen under docetaxel treatment pressure. We identified 17 candidate genes whose suppression may enhance the efficacy of docetaxel, with transcription elongation factor A-like 1 (Tceal1) as the top candidate. TCEAL1 function is not fully characterised; it may modulate transcription in a promoter dependent fashion. Suppressed TCEAL1 expression in multiple human prostate cancer cell lines enhanced therapeutic response to docetaxel. Based on gene set enrichment analysis from transcriptomic data and flow cytometry, we confirmed that loss of TCEAL1 in combination with docetaxel leads to an altered cell cycle profile compared with docetaxel alone, with increased subG1 cell death and increased polyploidy. Here, we report the first in vivo genome-wide treatment sensitisation CRISPR screen in prostate cancer, and present proof of concept data on TCEAL1 as a candidate for a combinational strategy with the use of docetaxel.

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CD4 T cell activating neoantigens enhance personalized cancer vaccine efficacy

Project description:CD4 T cell activating neoantigens enhance personalized cancer vaccine efficacy

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Genome-Wide CRISPR Screen Identifies Multiple Synthetic Lethal Targets That Enhance KRAS (G12C) Inhibitor Efficacy

Project description:Genome-Wide CRISPR Screen Identifies Multiple Synthetic Lethal Targets That Enhance KRAS (G12C) Inhibitor Efficacy

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Expression data from prostate cancer cell lines C4-2B (docetaxel sensitive) and TaxR (docetaxel resistant) cells

Project description:Prostate cancer C4-2B cells were cultured in docetaxel in a dose-escalation manner. After nine months selection, cells were able to divide freely in 5 nM docetaxel, with a specific sets of genes been deregulated. We performed global gene expression analysis by cDNA microarrays to identify genes responsible for docetaxel resistance in TaxR cells. Docetaxel resistant TaxR cells were selected from C4-2B cells during long time docetaxel treatment. Genes responsible for docetaxel resistance were identified using C4-2B vs. TaxR RNA extraction and hybridization on Affymetrix microarrays.

2013-08-01 | E-GEOD-47040 | biostudies-arrayexpress

Expression data from prostate cancer cell lines C4-2B (docetaxel sensitive) and TaxR (docetaxel resistant) cells

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Genome-Wide CRISPR Screen Identifies Multiple Synthetic Lethal Targets That Enhance KRAS (G12C) Inhibitor Efficacy [CRISPR]

Project description:Genome-Wide CRISPR Screen Identifies Multiple Synthetic Lethal Targets That Enhance KRAS (G12C) Inhibitor Efficacy [CRISPR]

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Identificatinon of differentially expressed genes in Docetaxel-resistant cell lines PC3 and DU145 after combination treatment with RU486 and docetaxel

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