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A genome-wide CRISPR screen identifies mediators of ferroptosis sensitivity in clear-cell carcinomas

ABSTRACT: A genome-wide CRISPR screen identifies mediators of ferroptosis sensitivity in clear-cell carcinomas

PROVIDER: PRJNA523003 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8587694.fastq.gz	Fastqsanger.gz
	SRR8587695.fastq.gz	Fastqsanger.gz
	SRR8587696.fastq.gz	Fastqsanger.gz
	SRR8587697.fastq.gz	Fastqsanger.gz

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A genome-wide CRISPR screen identifies mediators of ferroptosis sensitivity in clear-cell carcinomas

Project description:Clear-cell carcinomas (CCCs) are a histological group of highly aggressive malignancies commonly originating in the kidney and ovary. CCC tumors are distinguished by aberrant lipid and glycogen accumulation and are inherently refractory to a broad range of anti-cancer therapies. In the study associated with this dataset, we identified an intrinsic vulnerability to ferroptosis associated with the unique metabolic state in CCC cells. However, the mediators of this sensitivity to ferroptosis are unknown. Here we perform a genome-wide CRISPR screen to identify genes that mediate the sensitivity to ML210, a selective inhibitor of glutathione peroxidase 4 (GPX4) and a potent inducer of ferroptotic cell death in 786-O, a clear-cell renal cell carcinoma cell line.

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A genome-wide CRISPR screen identifies mediators of ferroptosis sensitivity in polyunsaturated fatty acid-treated cells

Project description:Polyunsaturated fatty acids (PUFA) sensitize cells to ferroptotic cell death. In the study associated with this dataset, we used UACC257 as a model cell line (intrinsically resistant to ferroptosis) induced to be sensitive to ferroptosis with different PUFAs. We performed genome-wide CRISPR knockout screen to identify genes that mediate the sensitivity to ML210, a selective inhibitor of glutathione peroxidase 4 (GPX4) and a potent inducer of ferroptotic cell death. We identified cytochrome P450 oxidoreductase (POR, CYPOR) as a key player required for ferroptotic cell death among other genes.

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Project description:A genome-wide CRISPR screen identifies mediators of ferroptosis sensitivity in polyunsaturated fatty acid-treated cells

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Project description:Ferroptosis is a form of regulated necrotic cell death controlled by glutathione peroxidase 4 (GPX4). At present, mechanisms that could predict sensitivity and/or resistance and that may be exploited to modulate this form of cell death are needed. We applied two independent approaches, a genome-wide CRISPR-based genetic screen and microarray analysis of ferroptosis-resistant cell lines to uncover acyl-CoA synthetase long-chain family member 4 (Acsl4) as an essential component for ferroptosis execution.

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IRF8 regulates intrinsic ferroptosis through repressing p53 expression to maintain tumor cell sensitivity to cytotoxic T lymphocytes

Project description:Ferroptosis has emerged as a cytotoxic T lymphocyte (CTL)-induced tumor cell death pathway. The regulation of tumor cell sensitivity to ferroptosis is still incompletely understood. We report here that the interferon regulatory factor 8 (IRF8) functions as a regulator of tumor cell intrinsic ferroptosis. Genome-wide gene expression profiling identified ferroptosis pathway as an IRF8-regulated pathway in tumor cells. IRF8.KO tumor cells acquire resistance to intrinsic ferroptosis induction and IRF8-deficient tumor cells exhibit decreased ferroptosis in response to tumor-specific CTLs. Irf8 deletion increases p53 expression in tumor cells and knocking out p53 in IRF8.KO tumor cells restored tumor cell sensitivity to intrinsic ferroptosis induction. Furthermore, IRF8.KO tumor cells grew significantly faster than WT tumor cells in immune competent mice. To restore IRF8 expression in tumor cells, we designed and synthesized codon usage-optimized IRF8-encoding DNA to generate IRF8-encoding plasmid NTC9385R-mIRF8. Restoring IRF8 expression via a lipid nanoparticle-encapsulated NTC9385R-mIRF8 plasmid therapy suppressed established tumor growth in vivo. In human cancer patients, nivolumab responders have a significant higher IRF8 expression level in their tumor cells as compared to the non-responders. Our data determine that IRF8 represses p53 expression to maintain tumor cell sensitivity to intrinsic ferroptosis

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