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Expression data from Che-1 (AATF) depleted SKBR3 and MDA-468 cell lines

ABSTRACT: Che-1 is a RNA Polymerase II binding protein involved in the regulation of gene transcription. We have observed that Che-1 depletion induces apoptosis in several cancer cells expressing mutated forms of p53. We used microarrays to investigate classes of genes regulated by Che-1 in one of these cell lines.

ORGANISM(S): Homo sapiens

PROVIDER: GSE20622 | GEO | 2010/03/05

SECONDARY ACCESSION(S): PRJNA124809

REPOSITORIES: GEO

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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

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

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Che-1/AATF-induced transcriptionally active chromatin promotes cell proliferation in Multiple Myeloma

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

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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]

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AATF interactome in human Kms27 cells

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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]

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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.

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Che-ating death: CHE1/AATF protects from p53-mediated apoptosis.

Project description: Not available

| S-EPMC3474930 | biostudies-other