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Mus musculus

ABSTRACT: BET-Bromodomain Inhibitors Engage The Host Immune System And Regulate Expression Of The Immune Checkpoint Ligand PD-L1 [EuMyc_RNA-seq]

OTHER RELATED OMICS DATASETS IN: GSE94057GSE94134

PROVIDER: PRJNA369041 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5208880_1.fastq.gz	Fastqsanger.gz
	SRR5208880_2.fastq.gz	Fastqsanger.gz
	SRR5208881_1.fastq.gz	Fastqsanger.gz
	SRR5208881_2.fastq.gz	Fastqsanger.gz
	SRR5208882_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

BET-Bromodomain Inhibitors Engage The Host Immune System And Regulate Expression Of The Immune Checkpoint Ligand PD-L1

Project description:BET-Bromodomain Inhibitors Engage The Host Immune System And Regulate Expression Of The Immune Checkpoint Ligand PD-L1

| PRJNA369036 | ENA

BET-Bromodomain Inhibitors Engage The Host Immune System And Regulate Expression Of The Immune Checkpoint Ligand PD-L1 [3mRNA-seq]

Project description:BET-Bromodomain Inhibitors Engage The Host Immune System And Regulate Expression Of The Immune Checkpoint Ligand PD-L1 [3mRNA-seq]

| PRJNA368684 | ENA

Mus musculus

Project description:BET-Bromodomain Inhibitors Engage The Host Immune System And Regulate Expression Of The Immune Checkpoint Ligand PD-L1 [EuMyc_ChIP-seq]

| PRJNA369031 | ENA

BET-Bromodomain Inhibitors Engage The Host Immune System And Regulate Expression Of The Immune Checkpoint Ligand PD-L1 [EuMyc_ChIP-seq]

Project description:BET inhibitors (BETi) target bromodomain-containing proteins and are currently being evaluated as anti-cancer agents. We discovered that the maximal therapeutic effects of BETi in a Myc-driven B cell lymphoma model required an intact host immune system. Genome-wide analysis of the BETi induced transcriptional response identified the immune checkpoint ligand Cd274 (Pd-l1) as a Myc-independent, BETi target-gene. BETi directly repressed constitutively expressed and IFN-γ induced CD274 expression across different human and mouse tumor cell lines and primary patient samples. Mechanistically, BETi decreased Brd4 occupancy at the Cd274 locus without any change in Myc occupancy, resulting in transcriptional pausing and rapid loss of Cd274 mRNA production. Finally, targeted inhibition of the PD1/PD-L1 axis by combining anti-PD1 antibodies and the BETi JQ1 caused synergistic responses in mice bearing Myc-driven lymphomas. Our data uncovers a novel interaction between BETi and the PD-1/PD-L1 immune-checkpoint and provides novel insight into the transcriptional regulation of CD274.

2017-02-01 | GSE94130 | GEO

BET-Bromodomain Inhibitors Engage The Host Immune System And Regulate Expression Of The Immune Checkpoint Ligand PD-L1 [EuMyc_RNA-seq]

2017-02-01 | GSE94133 | GEO

BET-Bromodomain Inhibitors Engage The Host Immune System And Regulate Expression Of The Immune Checkpoint Ligand PD-L1 [3mRNA-seq]

2017-02-01 | GSE94057 | GEO

Application of peptide barcoding to obtain high-affinity anti-PD-1 nanobodies

Project description:Cancer treatment has been revolutionized by immune checkpoint inhibitors, which regulate immune cell function by blocking the interactions between immune checkpoint molecules and their ligands. The interaction between programmed cell death-1 (PD-1) and programmed cell death-ligand 1 (PD-L1) is a target for immune checkpoint inhibitors. Nanobodies, which are recombinant variable domains of heavy-chain-only antibodies, can replace existing immune checkpoint inhibitors, such as anti-PD-1 or anti-PD-L1 conventional antibodies. However, the screening process for high-affinity nanobodies is laborious and time-consuming. Here, we identified high-affinity anti-PD-1 nanobodies using peptide barcoding, which enabled reliable and efficient screening by distinguishing each nanobody with a peptide barcode that was genetically appended to each nanobody. We prepared a peptide-barcoded nanobody (PBNb) library with thousands of variants. Three high-affinity PBNbs were identified from the PBNb library by quantifying the peptide barcodes derived from high-affinity PBNbs. Furthermore, these three PBNbs neutralized the interaction between PD-1 and PD-L1. Our results demonstrate the utility of peptide barcoding and the resulting nanobodies can be used as experimental tools and antitumor agents. Peptide barcoding can be used to screen for molecules other than nanobodies. Our methods, such as the design of peptide barcodes, the design of peptide-barcoded molecules, preparation of peptide-barcoded molecule library, and quantification of peptide barcodes, are helpful in screening for peptide-barcoded molecules.

2024-03-21 | PXD041000 | JPOST Repository

Epigenetic targeting of immunocheckpoint PD-L1 by BET bromodomain inhibition

Project description:Epigenetic regulators have emerged as exciting targets for cancer therapy. Additionally, restoration of antitumor immunity by blocking the PD-L1 signaling using antibodies has proven to be beneficial in cancer therapy. Here we show that BET bromodomain inhibition suppresses PD-L1 expression and restores antitumor immunity in ovarian cancer. CD274 (encoding PD-L1) is a direct target of BRD4-mediated gene transcription. In mouse models, treatment with the BET inhibitor JQ1 significantly reduced PD-L1 expression on tumor cells and tumor-associated dendritic cells and macrophages, which correlated with an increase in the activity of antitumor cytotoxic T cells. Together, these data demonstrate an epigenetic approach to block PD-L1 signaling to restore antitumor immunity. Given the fact that BET inhibitors have been proven safe with manageable reversible toxicity in clinical trials, our findings indicate that pharmacological BET inhibitors represent a novel treatment strategy for targeting PD-L1 expression.

2016-10-17 | GSE81698 | GEO

Therapeutic Targeting of the p300/CBP Bromodomain Enhances the Efficacy of Immune Checkpoint Blockade Therapy

Project description:Blockade of immune checkpoints, such as programmed death-ligand 1 (PD-L1), has shown promise in cancer treatment; however, clinical response remains limited in many cancer types. Our previous research demonstrated that p300/CBP mediates the acetylation of the PD-L1 promoter, regulating PD-L1 expression. In this study, we further investigated the role of the p300/CBP bromodomain in regulating PD-L1 expression using CCS1477, a selective bromodomain inhibitor developed by our team. We found that the p300/CBP bromodomain is essential for H3K27 acetylation at PD-L1 enhancers. Inhibiting this modification significantly reduced enhancer activity and PD-L1 transcription, including exosomal PD-L1, which has been implicated as key contributors to resistance against PD-L1 blockade therapy in various cancers. Furthermore, CCS1477 treatment resulted in a marked reduction of myeloid-derived suppressor cells (MDSCs) in the tumor microenvironment (TME) by inhibiting key cytokines such as IL6, CSF1, and CSF2, which are crucial for MDSC differentiation and recruitment. By reducing PD-L1 expression and modulating the immunosuppressive TME, CCS1477 creates a more favorable environment for tumor-infiltrating lymphocytes, significantly enhancing the efficacy of immune checkpoint blockade (ICB) therapy. Notably, these effects were observed in both prostate cancer and melanoma models, underscoring the broad therapeutic potential of p300/CBP bromodomain inhibition in improving ICB outcomes.

2025-08-27 | GSE291279 | GEO

Anti-PD-L1 antibodies exacerbate arthritis and pain via increased production of CXCL8/IL-8 and FGF9 in synovial fibroblasts

Project description:Immune checkpoint inhibitors (ICIs) in cancer therapy are challenged for immune-related adverse events (irAEs), such as inflammatory arthritis induced by ICI therapy (ICI-arthritis) and exacerbation of rheumatoid arthritis (RA). As well as activating T cells by inhibiting programmed cell death protein 1 (PD-1)/ programmed death ligand 1 (PD-L1) signal, anti-PD-L1 antibody (αPD-L1 ab) activate intracellular pathway through PD-L1 binding. However, the effects of αPD-L1 ab on synovial fibroblasts, which are important in the pathogenesis of arthritis, are unknown.

2025-07-11 | GSE272100 | GEO

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