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ABSTRACT: Saturation genome editing of DDX3X clarifies pathogenicity of germline and somatic variation

PROVIDER: PRJEB52900 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR9741180_1.fastq.gz	Fastqsanger.gz
	ERR9741180_2.fastq.gz	Fastqsanger.gz
	ERR9741190_1.fastq.gz	Fastqsanger.gz
	ERR9741190_2.fastq.gz	Fastqsanger.gz
	ERR9741200_1.fastq.gz	Fastqsanger.gz

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Project description:Accumulating evidence has shown that cellular double-stranded RNAs (dsRNAs) induce antiviral innate immune responses in human normal and malignant cancer cells. However, it is not fully understood how endogenous ‘self’ dsRNA homeostasis is regulated in the cell. Here, we show that an RNA-binding protein, DEAD-box RNA helicase 3X (DDX3X), prevents the aberrant accumulation of cellular dsRNAs. Loss of DDX3X induces dsRNA sensor-mediated type I interferon signaling and innate immune response in breast cancer cells due to abnormal cytoplasmic accumulation of dsRNAs. Dual depletion of DDX3X and a dsRNA-editing protein, ADAR1 synergistically activates the cytosolic dsRNA pathway in breast cancer cell. Moreover, inhibiting DDX3X enhances the antitumor activity by increasing tumor intrinsic-type I interferon response, antigen presentation, and tumor-infiltration of cytotoxic T cells as well as dendritic cells in breast tumors, which may lead to the development of breast cancer therapy by targeting DDX3X in combination with immune checkpoint blockade. To assess the impact of DDX3X on the gene expression in the breast cancer, we stably depleted DDX3X in breast cancer MCF7 cells using a short hairpin RNA (shRNA)-mediated knockdown, and performed a genome-wide transcriptome analysis using a next-generation RNA deep sequencing.

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