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ChIPseq of DDX3X, DDX54, ER and H3K4me3 in human MCF7 cells

ABSTRACT: ChIPseq of DDX3X, DDX54, ER and H3K4me3 in human MCF7 cells

PROVIDER: PRJEB23458 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR2195860.fastq.gz	Fastqsanger.gz
	ERR2195870.fastq.gz	Fastqsanger.gz
	ERR2195861.fastq.gz	Fastqsanger.gz
	ERR2195871.fastq.gz	Fastqsanger.gz
	ERR2195862.fastq.gz	Fastqsanger.gz

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ChIPseq of DDX3X, DDX54, ERalpha and H3K4me3 in human breast cancer MCF7 cells

Project description:We aimed to investigate the chromatin binding activity of DDX3X and DDX54 RNA helicases in human ER -dependent breast cancer MCF7 cells. We run a parallel chromatin binding profiling of ER ChIP-seq. H3K4me3 profiling was used as a quality control of the ChIP-seq procedure.

2019-11-14 | E-MTAB-6211 | biostudies-arrayexpress

Expression profiling of DDX3X and DDX54 knockdown in MCF7 cells

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Project description:Individual nucleotide resolution cross-linking immunoprecipitation (iCLIP) detects protein-RNA binding sites at a single nucleotide resolution. We aimed to identify the transcripts directly bound to DDX3X and DDX54 in human breast cancer MCF7 cells and to characterize the site of interaction at a single nucleotide resolution.

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PARP-1, H3 and H3K4me3 ChIP-chip from MCF7 cells

Project description:We are examining the mechanisms by which the nuclear enzyme PARP-1 regulates gene expression. We performed ChIP-chip for PARP-1, histone H3 and H3K4me3 (lysine 4 trimethylation on histone H3) in MCF7 breast carcinoma cells, and looked at 23550 RefSeq genes to determine binding patterns of these factors at promoters. Each experiment was performed in duplicate. ChIP-chip biological replicates for PARP-1, H3 and H3K4me3 (2 replicates each) from MCF7 human breast carcinoma cells are included.

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Inhibiting DDX3X triggers tumor-intrinsic type I interferon response and enhances anti-tumor immunity

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.

2020-09-03 | GSE157323 | GEO

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