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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]

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

ORGANISM(S): Mus musculus

PROVIDER: GSE120517 | 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. [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]

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]

2021-06-07 | GSE100494 | 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

| PRJNA392414 | ENA

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

Project description:Multiple myeloma (MM) is a blood disease characterized by the malignant accumulation of monoclonal plasma cells in the bone marrow. Among the pathological consequences of the MM, defects in osteogenesis characterized by osteolytic lesions, osteopenia, and pathologic fractures are frequently described. Che-1/AATF (Che-1) is a co-transcriptional factor involved in MM transformation and proliferation. Here, we show that Che-1 expression in MM contributes to maintaining low level of WWTR1 (TAZ), a transcriptional coactivator downstream of the Hippo-signaling pathway. We report that the miR-590-3p, deriving from the mRNA splicing of the EIF4H host gene, can target TAZ, contributing to downregulating its expression in MM. Furthermore, we demonstrate by in vivo and in vitro experiments that Che-1 transcriptionally induces EIF4H gene. We provide data to support that miR-590-3p is secreted by MM cells in vitro and in vivo and that can inhibit TAZ levels and the physiological transcriptional expression of osteogenic-related genes, in mesenchymal stem cells. Our findings unveil an unexplored novel Che-1/miR-590-3p/TAZ axis in MM tumorigenesis by providing a rationale to explore the therapeutic potential of metastatic bone lesions.

2024-04-10 | GSE234642 | GEO

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

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

2021-06-07 | GSE100647 | 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:Che-1/AATF sustains cell growth and global transcription in Multiple Myeloma through the maintenance of open chromatin structure. [RNA-Seq, mouse]

| PRJNA493252 | ENA

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

Expression data from Che-1 (AATF) depleted HCT 116 cell line

Project description:Che-1 is a RNA Polymerase II binding protein involved in the regulation of gene transcription. Che-1 emerges as an important adaptor that connects transcriptional regulation, cell-cycle progression, checkpoint control, and apoptosis. We have observed that Che-1 depletion sensitizes cells to chemotherapy. We used microarrays analysis to investigate classes of genes regulated by Che-1. Total RNA was extracted from control and Che-1 depleted HCT 116 cells 48 hours after transient transfection of siRNA.

2013-03-12 | E-GEOD-45009 | biostudies-arrayexpress

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