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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE97484 | GEO | 2017/12/07

SECONDARY ACCESSION(S): PRJNA381950

REPOSITORIES: GEO

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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

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

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

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

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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.

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Male SD rats treated with high fat diet (HFD) and DNA methyltransferase (DNMT) inhibitor 5-aza-2'-deoxycytidine (5-AzaD)

Project description:This SuperSeries is composed of the SubSeries listed below.

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Reduced representation bisulfite sequencing (RRBS) of xenografts of mouse breast cancer cell line treated with C29, 5-aza-2'-deoxycytidine or a combination of both

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