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Regulatin of KDM5C stability and enhancer reprogramming in breast cancer

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

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE185836 | GEO | 2022/10/27

REPOSITORIES: GEO

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Regulation of KDM5C stability and enhancer reprogramming in breast cancer.

Project description:Abnormality of enhancer regulation has emerged as one of the critical features for cancer cells. KDM5C is a histone H3K4 demethylase and frequently mutated in several types of cancer. It is critical for H3K4me3 and activity of enhancers, but its regulatory mechanisms remain elusive. Here, we identify TRIM11 as one ubiquitin E3 ligase for KDM5C. TRIM11 interacts with KDM5C, catalyzes K48-linked ubiquitin chain on KDM5C, and promotes KDM5C degradation through proteasome. TRIM11 deficiency in an animal model represses the growth of breast tumor and stabilizes KDM5C. In breast cancer patient tissues, TRIM11 is highly expressed and KDM5C is lower expressed, and their expression is negatively correlated. Mechanistically, TRIM11 regulates the enhancer activity of genes involved in cell migration and immune response by targeting KDM5C. TRIM11 and KDM5C regulate MCAM expression and cell migration through targeting H3K4me3 on MCAM enhancer. Taken together, our study reveals novel mechanisms for enhancer regulation during breast cancer tumorigenesis and development.

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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

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

Project description: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.

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The role of histone demethylase KDM5C in super-enhancer activation

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

2017-07-19 | GSE101565 | GEO

Enhancer reprogramming promotes pancreatic cancer progression and metastasis

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2017-07-31 | GSE99311 | GEO

Enhancer reprogramming driven by high-order assemblies of transcription factors promotes phenotypic plasticity and breast cancer endocrine resistance

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

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