Proteasome inhibition reprograms chromatin landscape in breast cancer (ChIP-Seq)
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1008754 | ENA |
REPOSITORIES: ENA
Dataset's files
| 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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Project description:Proteasome inhibition reprograms chromatin landscape in breast cancer
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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
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 | GSE241599 | GEO
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 | GSE241598 | GEO
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 | GSE241597 | GEO
Project description:The 26S proteasome is the major protein degradation machinery in cells. Cancer cells use the proteasome to modulate gene expression networks that promote tumor growth. Proteasome inhibitors have emerged as effective cancer therapeutics, but how they work mechanistically remains unclear. Here, using integrative genomic analysis, we discovered unexpected reprogramming of the chromatin landscape and RNA polymerase II (RNAPII) transcription initiation in breast cancer cells treated with the proteasome inhibitor MG132. The cells acquired dynamic changes in chromatin accessibility at specific genomic loci termed differentially open chromatin regions (DOCR). DOCRs with decreased accessibility were promoter proximal and exhibited unique chromatin architecture associated with divergent RNAPII transcription. Conversely, DOCRs with increased accessibility were primarily distal to transcription start sites and enriched in oncogenic superenhancers predominantly accessible in non-basal breast tumor subtypes. These findings describe the mechanisms by which the proteasome modulates the expression of gene networks intrinsic to breast cancer biology.SignificanceOur study provides a strong basis for understanding the mechanisms by which proteasome inhibitors exert anticancer effects. We find open chromatin regions that change during proteasome inhibition, are typically accessible in non-basal breast cancers.
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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