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Che-1/AATF sustains cell growth and global transcription in Multiple Myeloma through the maintenance of open chromatin structure

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

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE100647 | GEO | 2021/06/07

REPOSITORIES: GEO

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Che-1/AATF sustains cell growth and global transcription in Multiple Myeloma through the maintenance of open chromatin structure [RNA-Seq]

Project description:Tumor transformation is the result of genetic modifications that alter gene transcription, thus producing a specific oncogenic program. However, in recent years, several exciting discoveries have shown that also aberrant epigenetic modifications play a major role in the genesis and progression of cancer. Multiple myeloma (MM) is a cancerous pathology resulting from the clonal expansion of plasma cells, and characterized by abnormal production and secretion of antibody proteins. This disease shows a great heterogeneity, caused by both genetic and epigenetic abnormalities, and despite the numerous therapeutic advances remains an incurable pathology. Here we show that the RNA Polymerase II binding protein, Che-1/AATF is required for MM cells growth by sustaining genome wide transcription and the recruitment of Pol II to the DNA. Notably, we found that Che-1 localizes on active chromatin and its depletion leads to accumulation of heterochromatin by a global decrease of histone acetylation. Moreover, we show that Che-1 directly interacts with histones and competes with HDAC class I members for histones binding. Strikingly, Che-1 downregulation decreases BRD4 chromatin accumulation and further sensitize MM cells to bromodomain and extra-terminal (BET) inhibitors. Overall, our findings identify an essential role of Che-1 in maintaining open chromatin required for sustaining MM growth, and support Che-1 as a possible target for MM therapy, alone or in combination with BET inhibitors.

2021-06-07 | GSE100493 | GEO

Che-1/AATF sustains cell growth and global transcription in Multiple Myeloma through the maintenance of open chromatin structure [ChIP-Seq]

2021-06-07 | GSE100646 | GEO

Che-1/AATF sustains cell growth and global transcription in Multiple Myeloma through the maintenance of open chromatin structure [ATAC-Seq]

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Che-1/AATF sustains cell growth and global transcription in Multiple Myeloma through the maintenance of open chromatin structure. [ATAC-Seq, mouse]

Project description:This series contains the ATAC-seq data for control and Che-1 silencing in the Multiple Myeloma mice model.

2021-06-07 | GSE120964 | GEO

Che-1/AATF sustains cell growth and global transcription in Multiple Myeloma through the maintenance of open chromatin structure. [RNA-Seq, mouse]

Project description:This series contains the transcriptomic profiling for control and Che-1 silencing in the Multiple Myeloma mice model’s.

2021-06-07 | GSE120517 | GEO

Che-1/AATF sustains cell growth and global transcription in Multiple Myeloma through the maintenance of open chromatin structure

Project description:Che-1/AATF sustains cell growth and global transcription in Multiple Myeloma through the maintenance of open chromatin structure

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Che-1/AATF-induced transcriptionally active chromatin promotes cell proliferation in multiple myeloma.

Project description:Multiple myeloma (MM) is a hematologic malignancy produced by a clonal expansion of plasma cells and characterized by abnormal production and secretion of monoclonal antibodies. This pathology exhibits an enormous heterogeneity resulting not only from genetic alterations but also from several epigenetic dysregulations. Here we provide evidence that Che-1/AATF (Che-1), an interactor of RNA polymerase II, promotes MM proliferation by affecting chromatin structure and sustaining global gene expression. We found that Che-1 depletion leads to a reduction of "active chromatin" by inducing a global decrease of histone acetylation. In this context, Che-1 directly interacts with histones and displaces histone deacetylase class I members from them. Strikingly, transgenic mice expressing human Che-1 in plasma cells develop MM with clinical features resembling those observed in the human disease. Finally, Che-1 downregulation decreases BRD4 chromatin accumulation to further sensitize MM cells to bromodomain and external domain inhibitors. These findings identify Che-1 as a promising target for MM therapy, alone or in combination with bromodomain and external domain inhibitors.

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Che-1/AATF sustains cell growth and global transcription in Multiple Myeloma through the maintenance of open chromatin structure. [RNA-Seq, mouse]

Project description:Che-1/AATF sustains cell growth and global transcription in Multiple Myeloma through the maintenance of open chromatin structure. [RNA-Seq, mouse]

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Che-1/AATF sustains cell growth and global transcription in Multiple Myeloma through the maintenance of open chromatin structure. [ATAC-Seq, mouse]

Project description:Che-1/AATF sustains cell growth and global transcription in Multiple Myeloma through the maintenance of open chromatin structure. [ATAC-Seq, mouse]

| PRJNA495146 | ENA

Che-1/miR-590-3p/TAZ axis sustains multiple myeloma disease.

Project description: Not available

| S-EPMC10997508 | biostudies-literature