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Breast cancer cells treated with a novel KDM5 inhibitor, 5-aza-2' Deoxycytidine, or both.

ABSTRACT: Breast cancer cells treated with a novel KDM5 inhibitor, 5-aza-2' Deoxycytidine, or both.

PROVIDER: PRJNA381950 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5427910.fastq.gz	Fastqsanger.gz
	SRR5427911.fastq.gz	Fastqsanger.gz
	SRR5427912.fastq.gz	Fastqsanger.gz
	SRR5427913.fastq.gz	Fastqsanger.gz
	SRR5427914.fastq.gz	Fastqsanger.gz

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Gene Expression profiling in luminal breast cancer cells treated with a novel KDM5 inhibitor, 5-aza-2' Deoxycytidine, or both.

2017-12-08 | GSE97482 | GEO

DNA Methylation profiling in luminal breast cancer cells treated with a novel KDM5 inhibitor, 5-aza-2' Deoxycytidine, or both.

Project description:Recently, the H3K4 demethylase, KDM5B, was shown to be amplified and overexpressed in luminal breast cancer, suggesting it might constitute a potential cancer therapy target. Here, we characterize, in breast cancer cells, the molecular effects of a recently developed small-molecule inhibitor of the KDM5 family of proteins, either alone, or in combination with the DNA demethylating agent 5-aza-2’ deoxycytidine (DAC). Alone, the KDM5 inhibitor (KDM5i) increased expression of a small number of genes, but when combined with DAC, the drug enhanced the effects of the latter for increasing expression of hundreds of DAC responsive genes. To determine if this combinatorial action was the result of enhanced DNA demethylation, we profiled genome-wide DNA methylation in cells treated with KDM5i, DAC, or both. Methylation levels at approximately 450,000 unique CpG loci were detected using the Infinium Illumina HumanMethylation 450 array. We found that KDM5i did not significantly affect DNA methylation either alone, or in combination with DAC.

2017-12-08 | GSE97483 | GEO

ChIP-seq analysis of H3K4me3 and H3K27ac localization in breast cancer cells treated with a novel KDM5 inhibitor, , 5-aza-2' Deoxycytidine, or both

Project description:Recently, the H3K4 demethylase, KDM5B, was shown to be amplified and overexpressed in luminal breast cancer, suggesting it might constitute a potential cancer therapy target. Here, we characterize, in breast cancer cells, the molecular effects of a recently developed small-molecule inhibitor of the KDM5 family of proteins, either alone, or in combination with the DNA demethylating agent 5-aza-2’ deoxycytidine (DAC). Alone, the KDM5 inhibitor (KDM5i) increased expression of a small number of genes, but when combined with DAC, the drug enhanced the effects of the latter for increasing expression of hundreds of DAC responsive genes. ChIP-seq studies revealed that KDM5i resulted in the broadening of existing, and creation of thousands of new H3K4me3 domains. When compared to DAC alone, increased promoter and gene body H3K4me3 occupancy at DAC responsive genes was observed in cells treated with the drug combination. Importantly, treatment with either DAC or DAC+KDM5i induced a dramatic increase in H3K27ac at enhancers with an associated significant increase in target gene expression, suggesting a previously unappreciated effect of DAC on transcriptional regulation. Finally, we found that KDM5i could synergize with DAC to reduce the viability of luminal breast cancer cells in in-vitro assays. Our study provides the first look into the molecular effects of novel KDM5i compounds and suggests that combining these with DAC may represent an exciting new approach to epigenetic therapy.

2017-12-08 | GSE97481 | GEO

MCF7 cells gene expression change by inducing CpG demethylation using 5-Aza-2'-deoxycytidine (Aza)

2011-08-18 | GSE31441 | GEO

SUMO pulldown proteomics Namalwa 5-Aza-2' deoxycytidine treatment

Project description:Combination therapies targeting malignancies aim to increase treatment efficacy and reduce toxicity. Hypomethylating drug 5-Aza-2’-deoxycytidine (5-Aza-2’) enhances transcription of tumor suppressor genes and induces replication errors via entrapment of DNMT1. Post-translational modification by SUMO plays major roles in the DNA damage response and is required for degradation of entrapped DNMT1. Here, we combine SUMOylation inhibitor TAK981 and DNA-hypomethylating agent 5-Aza-2’ to improve treatment of MYC driven hematopoietic malignancies, since MYC overexpressing tumors are sensitive to SUMOylation inhibition. We studied the classical MYC driven malignancy Burkitt lymphoma, as well as diffuse large B-cell lymphoma (DLBCL) with and without MYC translocation. SUMO inhibition prolonged the entrapment of DNMT1 to DNA, resulting in DNA damage. An increase in DNA damage was observed in cells co-treated with TAK981 and 5-Aza-2’. Both drugs synergized to reduce cell proliferation in vitro in a B cell lymphoma cell panel, including Burkitt lymphoma and DLBCL. In vivo experiments combining TAK981 (25 mg/kg) and 5-Aza-2’ (2.5 mg/kg) showed a significant reduction in outgrowth of Burkitt lymphoma in an orthotopic xenograft model. In contrast, single dosing of TAK981 was ineffective and single dosing of 5-Aza-2’ only led to a modest outgrowth reduction. TAK981 and 5-Aza-2’ synergize to reduce B cell Lymphoma outgrowth in vitro and in vivo. SUMOylation is a key-player in the repair of DNA damage, hence upon TAK981 treatment the repair of DNA damage induced by 5-Aza-2’ treatment is impaired. Our results demonstrate the potential of tailored combination of drugs, based on insight in molecular mechanisms, to improve the efficacy of cancer therapies.

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MCF7 cells gene expression change by inducing CpG demethylation using 5-Aza-2'-deoxycytidine (Aza)

Project description:Promoter methylation is able to induce downregulation of gene expression. 5-Aza-2'-deoxycytidine(Aza), methytransferase inhibitor, induce CpG demethylation. Here, 5-Aza-2'-deoxycytidine(Aza) is treated in a human breast cancer cell, MCF7, for detection of gene expression change. To analyze gene expression change by aza, control RNA isolated from MCF-7 was compared with RNA isolated from MCF-7 treated with 5uM and 10uM aza.

2011-08-17 | E-GEOD-31441 | biostudies-arrayexpress

SUMO pulldown, U2OS, proteomics, 4 hour 20 hour 5-Aza-2' deoxycytidine treatment

2023-03-17 | PXD038617 | Pride

5-aza-2-deoxycytidine treatment of Swarm rat chondrosarcoma cells

Project description:The puropose of this experiment was to identify gene expression changes that result from 5-aza-2-deoxycytidine induced DNA demethylation of Swarm rat chondrosarcoma cells. The gene expression profiles of untreated Swarm rat chondrosarcoma cells were compared to the gene expression profiles of Swarm rat chondrosarcoma cells that were treated for 5 passages with a low dose of 5-aza-2-deoxycytidine (0.1uM).

2010-08-06 | GSE17598 | GEO

Expression microarray with 5-aza-2'-deoxycytidine-treated Caco-2 cells

Project description:5-aza-2'-deoxycytidine (DAC) treated and untreated Caco-2 cells were compared using an expression microarray.

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Genome-wide DNA demethylation of TGW (neuroblastoma cell line) after treatment of mock and 5-aza-2'-deoxycytidine (5-aza-dC)

Project description:A neuroblasoma cell line, TGW, was treated with a DNA demethylating agents (5-aza-2'-deoxycytidine: 5-aza-dC). Genome-wide DNA methylation was analyzed using the Infinium Human MethylationEPIC BeadChip.

2021-07-23 | GSE180660 | GEO

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