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IRF3 drives replication stress signaling and determines sensitivity to genotoxic agents in triple-negative breast cancer cells

ABSTRACT: IRF3 drives replication stress signaling and determines sensitivity to genotoxic agents in triple-negative breast cancer cells

PROVIDER: PRJNA1100437 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28764241_1.fastq.gz	Fastqsanger.gz
	SRR28764241_2.fastq.gz	Fastqsanger.gz
	SRR28764242_1.fastq.gz	Fastqsanger.gz
	SRR28764242_2.fastq.gz	Fastqsanger.gz
	SRR28764243_1.fastq.gz	Fastqsanger.gz

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IRF3 drives replication stress signaling and determines sensitivity to genotoxic agents in triple-negative breast cancer cells

Project description:Interferon-β signaling has been shown to play important roles in anti-virus as well as anti-tumor immunity. We here report that the key transcription factor in type I interferon signaling, IRF3, as well as downstream interferon-β are able to induce replication stress signaling in triple-negative breast cancer cells. IRF3 overexpression sensitizes triple-negative breast cancer cells to several genotoxic agents. Addition of IFN-β, a key downstream cytokine of IRF3,reduced replication fork speed and activated ATR-CHK1 signaling. Conversely, type I interferon-neutralizing antibodies or nucleosides supplementation rescued IRF3-induced replication stress.

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