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The Bromodomain and extraterminal (BET) inhibitor attenuates inflammatory response and cell migration in human microglia

ABSTRACT: We investigated the mechanisms underlying the anti-inflammatory and anti-migratory function and genes targeted by JQ1 in lipopolysaccharide (LPS)-activated human microglia HMC3 cells using RNA sequencing. The BET inhibitor JQ1 attenuates the LPS-induced inflammatory and migratory response. In addition, LPS-induced IRF1 was inhibited by JQ1, and IRF1 suppressed microglial migration by regulating inflammation and migration genes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE155408 | GEO | 2021/04/28

REPOSITORIES: GEO

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Selectively targeting bromodomain and extraterminal proteins for degradation as a novel anti-glioblastoma strategy [ChIP-seq]

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Targeting bromodomain and extraterminal proteins in breast cancer.

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Bromodomain and extraterminal proteins foster the core transcriptional regulatory programs and confer vulnerability in liposarcoma (ChIP-Seq)

Project description:Purpose: Identification of core transcriptional regulatory programs and bromodomain and extraterminal (BET) protein dependency in liposarcoma (LPS) Methods: ChIP-seq and RNA-seq were performed on LPS cells. Antibodies against H3K27ac, H3K4me1, H3K4me3, RNA-Pol2, BRD2, BRD3, BRD4, FOSL2, pan-RUNX, and DDIT3 (FUS-DDIT3) were used for ChIP-seq assays. The transcriptome responses of LPS141 and MLS402 cells to OTX015 and ARV-825 were compared. Result: We generated genome-wide chromatin-state maps of LPS cells. By charting the super-enhancer structures, we identify a bromodomain and extraterminal (BET) protein-cooperated FUS-DDIT3 function in myxoid LPS and a BET protein-dependent core transcriptional regulatory circuitry consisting of FOSL2, MYC, and RUNX1 in de-differentiated LPS. This study also provides a framework for discovering and targeting of core oncogenic transcriptional programs.

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Bromodomain and extraterminal proteins foster the core transcriptional regulatory programs and confer vulnerability in liposarcoma (RNA-Seq)

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The Bromodomain and extraterminal (BET) inhibitor attenuates inflammatory response and cell migration in human microglia

Project description:The Bromodomain and extraterminal (BET) inhibitor attenuates inflammatory response and cell migration in human microglia

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Bromodomain and Extraterminal Proteins as Novel Epigenetic Targets for Renal Diseases.

Project description:Epigenetic mechanisms, especially DNA methylation and histone modifications, are dynamic processes that regulate the gene expression transcriptional program in normal and diseased states. The bromodomain and extraterminal (BET) protein family (BRD2, BRD3, BRD4, and BRDT) are epigenetic readers that, via bromodomains, regulate gene transcription by binding to acetylated lysine residues on histones and master transcriptional factors. Experimental data have demonstrated the involvement of some BET proteins in many pathological conditions, including tumor development, infections, autoimmunity, and inflammation. Selective bromodomain inhibitors are epigenetic drugs that block the interaction between BET proteins and acetylated proteins, thus exerting beneficial effects. Recent data have described the beneficial effect of BET inhibition on experimental renal diseases. Emerging evidence underscores the importance of environmental modifications in the origin of pathological features in chronic kidney diseases (CKD). Several cellular processes such as oxidation, metabolic disorders, cytokines, inflammation, or accumulated uremic toxins may induce epigenetic modifications that regulate key processes involved in renal damage and in other pathological conditions observed in CKD patients. Here, we review how targeting bromodomains in BET proteins may regulate essential processes involved in renal diseases and in associated complications found in CKD patients, such as cardiovascular damage, highlighting the potential of epigenetic therapeutic strategies against BET proteins for CKD treatment and associated risks.

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