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Regulatin of KDM5C stability and enhancer reprogramming in breast cancer [ChIP-Seq]

ABSTRACT: We report the high-throughput profiling of histone modifications( H3K4me3 and H3K27ac) inTRIM11 knockdown and KDM5C knockdown MDA-MB-231 cells. we generated genome-wide chromatin-state maps of MDA-MB-231 cells.This study provides the localization of H3K4me3 and H3K27ac on chromatin in TRIM11 knockdown and KDM5C knockdown MDA-MB-231 cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE185832 | GEO | 2022/10/27

REPOSITORIES: GEO

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Regulatin of KDM5C stability and enhancer reprogramming in breast cancer [RNA-seq]

Project description:Purpose: Purpose:Exploring genes regulated by trim11 and kdm5c in breast cancer Methods: TRIM11 knock down and KDM5C knock down MDA-MB-231 cell lines were constructed and Trim11 knock down MMTV mice were generated. The RNA-seq libraries of cell lines and mice mammary tumors were sequenced by Illumina Nova-seq platform with pair-end reads of 150 bp. Results: Quality control of mRNA-seq data was performed using Fatsqc and low-quality bases were trimmed. The adaptor sequence was removed using Cutadapt (version 1.16) to clean RNA-seq raw data. All RNA-seq data were mapped to the human reference genome (hg19) or mouse reference genome (mm10) by HISAT2 (version 2.1.0). The gene expression level was calculated by Cufflinks with default parameters. Differential expressed genes (DEGs) were identified by 1.5-fold change and p-value < 0.05. Gene ontology analysis and KEGG pathways analysis was performed using DAVID (https://david.ncifcrf.gov). Conclusions: Our study represents biological process and KEGG pathway enrichment analyses of TRIM11 and KDM5C down-regulated genes or up-regulated genes

2022-10-27 | GSE185831 | GEO

The Kdm5c histone demethylase controls enhancer and promoter function.

Project description:Here, we show that the Kdm5c/Smcx member of the Jarid1 family of H3K4 demethylases is recruited to both enhancer and core promoter elements in ES and neuronal progenitor cells (NPC). Knockdown of Kdm5c deregulates transcription via a local increase in H3K4me3. While at core promoters the function of Kdm5c is to restrict transcription, loss of Kdm5c impairs enhancer function. Remarkably, an impaired enhancer function activates promoter activity from Kdm5c-bound intergenic regions. Our results demonstrate that the Kdm5c demethylase plays a crucial role in the functional identity and discrimination of enhancers and core promoters. We speculate that this is related to recruitment of H3K4me3 binders like the TFIID and NURF complexes6-8. Providing functional identity to genomic regions through balancing enzymes that deposit and remove histone modifications may prove to be a general epigenetic mechanism for the functional indexing of eukaryotic genomes. Examination of the KDM5C binding sites in mouse embryonic stem cells and in neuronal progenitor cells. Effect of KDM5C knock down on H3K4me3 and H3K4me1 levels and gene expression.

2013-04-01 | E-GEOD-34975 | biostudies-arrayexpress

NO001: Kdm5c controls promoter and enhancer activities

Project description:The functional organization of eukaryotic genomes correlates with specific patterns of histone methylations. Regulatory regions in genomes like enhancers and promoters differ in their extent of methylation of histone H3 at lysine-4 (H3K4), but it is largely unknown how the different methylation states are specified and controlled. Here, we show that the Kdm5c/Jarid1c/SMCX member of the Kdm5 family of H3K4 demethylases can be recruited to both enhancer and promoter elements in embryonic stem cells and neuronal progenitor cells via gene-specific transcription factors. Knockdown of Kdm5c deregulates transcription via local increases in H3K4me3. Our data show that restricting H3K4me3 modification at core promoters dampens transcription, but Kdm5c is required at enhancers for their full activity. Remarkably, an impaired enhancer function activates the intrinsic promoter activity of Kdm5c-bound distal elements. Our results demonstrate that the Kdm5c demethylase plays a crucial and dynamic role in the functional discrimination between enhancers and core promoters. RNA from four independent cultures from each sh Kdm5c #1, sh Kdm5c #2 and non-targeting shRNA polyclonal cell lines were hybridized in dye-swap against a common reference of RNA from IB10 ES cells.

2013-04-05 | E-GEOD-38862 | biostudies-arrayexpress

Cbx8 acts non-canonically with Wdr5 to promote mammary tumorigenesis [ChIP-Seq]

Project description:Here we found that Cbx8 knockdown in MMTV-Myc and MDA-MB-231-Luc cells reduces H3K4me3 mark on Notch-network genes

2016-06-21 | GSE71003 | GEO

Genome-wide maps of chromatin state in MDA-MB-231 cells [ChIP-seq]

Project description:We report a series of ChIP-Seq results in MDA-MB-231 cells. Briefly, we performed ChIP-Seq experiments with antibodies specific for PHF20L1, MTA1, EZH2, H3K27me2, H3K27me3 and H3K27ac in normal or knockdown of PHF20L1 MDA-MB-231 cells . We found that knockdown of PHF20L1 reduced the enrichment of MTA1, EZH2, H3K27me2, and H3K27me3 on the PHF20L1 target gene, and the enrichment of H3K27ac increased. This study gave us a new understanding of the role of PHF20L1 in chromatin status and gene transcription.

2020-03-12 | GSE128231 | GEO

The Histone Demethylase KDM5C Functions as a Tumor Suppressor in AML by Repression of B ivalently M arked Immature Genes

Project description:To uncover novel epigenetic regulators in AML, we performed an in vivo short hairpin RNA (shRNA) screen in the context of Cebpa mutant AML. This led to the identification of the Histone 3 Lysine 4 (H3K4) demethylase, KDM5C, as a novel tumor suppressor in AML. KDM5C potentially functions as a transcriptional repressor via its demethylase activity at promoters, and dysregulation could therefore have widespread consequences. Here, we found that reduced Kdm5c/KDM5C expression is associated with accelerated growth in both human and murine AML cell lines. In vivo, Kdm5c knockdown in a Cebpa mutant AML mouse model resulted in a more aggressive, immature and short-latency phenotype. Mechanistically, we show that knockdown of Kdm5c increased H3K4me3 globally. This translated into the up-regulation of a group of bivalently marked immature genes, resulting in a de-differentiation phenotype which could be reversed by modulating levels of pro-differentiation factors. Finally, we demonstrated that low levels of KDM5C were associated with a decrease in long-term disease-free survival, specifically in female patients. This emphasizes the clinical relevance of our findings and identifies KDM5C as a novel female-biased tumor suppressor in AML.

2023-03-10 | PXD016568 | Pride

Gene expression profile in breast cancer cells

Project description:We report the gene expression patterns in MDA-MB-231 (a line selected for low metastatic ability), MDA-MB-231-1833 (its bone-tropic metastatic derivative line), MDA-MB-231p27CK-DD (a phosphomimetic cell line), MDA-MB-231-1833shp27 (p27 knockdown cell line), MDA-MB-231-1833PF1502 (PI3K inhibitor treatment). It shows that the gene expression pattern are regulated in a p27 phosphorylation-dependent manner.

2019-03-19 | GSE112445 | GEO

LC-MSMS MDA-MB-231 with knockdown of ELOVL5 and IGFBP6 genes

Project description:Identification of changes in protein expression by label-free shotgun proteomics in breast cancer MDA-MB-231 cells with knockdown of ELOVL5 and IGFBP6 genes in comparison with control MDA-MB-231 cells.

2021-05-20 | PXD023892 | Pride

Identification of enhancer landscape in MDA-MB-231 cells

Project description:To identify typical enhancers and super-enhancers in the MDA-MB-231 triple-negative breast cancer cell line, we performed ChIP-seq using DNA isolated from untreated MDA-MB-231 cells using an H3K27ac antibody.

2020-02-21 | GSE95222 | GEO

Differential gene expression analysis of RNAseq data comparing control and srGAP1 knockdown MDA-MB-231 primary tumors.

Project description:To investigate the differential expression of genes in human tumor xenografts of control MDA-MB-231 primary tumors (Ctrl) and srGAP1 knockdown MDA-MB-231 primary tumors.

2022-08-10 | GSE210488 | GEO

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