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Proteasome inhibition reprograms chromatin landscape in breast cancer

ABSTRACT: Proteasome inhibition reprograms chromatin landscape in breast cancer

PROVIDER: PRJNA1008750 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25752134_1.fastq.gz	Fastqsanger.gz
	SRR25752134_2.fastq.gz	Fastqsanger.gz
	SRR25752135_1.fastq.gz	Fastqsanger.gz
	SRR25752135_2.fastq.gz	Fastqsanger.gz
	SRR25752136_1.fastq.gz	Fastqsanger.gz

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Proteasome inhibition reprograms chromatin landscape in breast cancer (Start-Seq)

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Proteasome inhibition reprograms chromatin landscape in breast cancer (ATAc-Seq)

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Proteasome inhibition reprograms chromatin landscape in breast cancer (ChIP-Seq)

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Proteasome inhibition reprograms chromatin landscape in breast cancer (RNA-Seq)

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Proteasome inhibition reprograms chromatin landscape in breast cancer (RNA-Seq)

Project description:The 26S proteasome regulates general protein homeostasis and controls vital cellular processes, including cell division and transcriptional regulation. Cancer cells are dependent on the proper functioning of the proteasome to modulate gene expression networks that promote tumor growth. Proteasome inhibition has emerged as an effective therapeutic strategy, although mechanisms by which this approach achieves its outcomes remain unclear. We performed an integrative analysis of the transcriptome and chromatin landscape of MCF-7 breast cancer cells treated with a model proteasome inhibitor, MG132, to examine the consequences of proteasome inhibition on gene regulation. MG132 treatment initiated dynamic changes in chromatin accessibility at specific loci termed Differentially Open Chromatin Regions (DOCRs). DOCRs with increased accessibility were primarily distal to transcription start sites (TSS), while those with decreased accessibility were promoter proximal and distal to TSS. Promoter proximal DOCRs showed a unique chromatin architecture associated with distinct divergent transcription patterns. Conversely, DOCRs distal to TSS were enriched in oncogenic super enhancers that are predominantly accessible in non-basal compared to basal breast tumor subtypes. These data define distinct chromatin states and RNAPII transcription patterns, revealing molecular mechanisms by which the proteasome modulates the expression of gene networks intrinsic to breast cancer biology.

2024-03-13 | GSE241600 | GEO

Proteasome inhibition reprograms chromatin landscape in breast cancer (Start-Seq)

2024-03-13 | GSE241599 | GEO

Proteasome inhibition reprograms chromatin landscape in breast cancer (ChIP-Seq)

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Proteasome inhibition reprograms chromatin landscape in breast cancer (ATAc-Seq)

2024-03-13 | GSE241597 | GEO

Proteasome inhibition blocks estrogen-dependent gene transcription by decreasing histone H2B monoubiquitination in human breast cancer cells

Project description:The estrogen receptor-alpha (ERα) determines breast cancer cell phenotype and is a prognostic indicator. A better understanding of the mechanisms controlling ERα function may uncover improved strategies for the treatment of breast cancer. Proteasome inhibition was previously reported to regulate estrogen-induced transcription but the mechanisms by which it influences ERα function remain controversial. In this study we investigated the transcriptome-wide effects of the proteasome inhibitor Velcade on estrogen-regulated transcription in MCF7 human breast cancer cells and demonstrate a specific global decrease in estrogen-induced transcription. This set contains 12 microarray samples. 3 controls, 3 estrogen stimulated, 3 Bortezomib stimulated, 3 Bortezomib + estrogen stimulated

2011-11-22 | E-GEOD-30931 | biostudies-arrayexpress

Cellular response to proteasome inhibition by Bortezomib

Project description:Analysis of the coordinated transcriptional reponse to proteasome inhibition mRNA profiles of NIH3T3 cells which stably expressing DD-sfGFP were generated by deep sequencing using Illumina HiSeq. The samples were collected from indicated timepoints after exposed to proteasome inhibition by Bortezomib.

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