ArticleScientific reports2018
Interplay between interferon regulatory factor 1 and BRD4 in the regulation of PD-L1 in pancreatic stellate cells.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 39 citations in OpenAlex.
- Low circulating miR-5193 promotes PD-L1-mediated immune evasion and relates to immune checkpoint inhibitor response in esophageal cancer.Molecular therapy. Nucleic acids · 2026Article
- Bi-directional regulation between NAD/NAMPT and IFN-γ/PD-L1 axes via BRD4/IRF1 and mitochondrial respiration in metastatic cutaneous melanoma.Journal of experimental & clinical cancer research : CR · 2026Article
- Overexpression of JMJD6 drives immune evasion via the BRD4-IRF1-PD-L1 axis and promotes malignancy in gastric cancer.Scientific reports · 2025Article
- Review
- Key role of interferon regulatory factor 1 (IRF-1) in regulating liver disease: progress and outlook.Journal of Zhejiang University. Science. B · 2024Review
- Statins abrogate gemcitabine-induced PD-L1 expression in pancreatic cancer-associated fibroblasts and cancer cells with improved therapeutic outcome.Cancer immunology, immunotherapy : CII · 2023Article
- Bromo- and Extra-Terminal Domain Inhibitors Induce Mitochondrial Stress in Pancreatic Ductal Adenocarcinoma.Molecular cancer therapeutics · 2023Article
- High Expression Level of BRD4 Is Associated with a Poor Prognosis and Immune Infiltration in Esophageal Squamous Cell Carcinoma.Digestive diseases and sciences · 2023Article
- Epigenetic regulation of pancreatic adenocarcinoma in the era of cancer immunotherapy.Journal of gastroenterology · 2022Review
- Neuronally expressed PDL1, not PD1, suppresses acute nociception.Brain, behavior, and immunity · 2022Article
- Review
- Inhibition of MNKs promotes macrophage immunosuppressive phenotype to limit CD8+ T cell antitumor immunity.JCI insight · 2022Article
- XP-524 is a dual-BET/EP300 inhibitor that represses oncogenic KRAS and potentiates immune checkpoint inhibition in pancreatic cancer.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Loss of SMAD4 Is Associated With Poor Tumor Immunogenicity and Reduced PD-L1 Expression in Pancreatic Cancer.Frontiers in oncology · 2022Article
- A New Trend in Cancer Treatment: The Combination of Epigenetics and Immunotherapy.Frontiers in immunology · 2022Review
- Review
- IRF1 regulates the progression of colorectal cancer via interferon‑induced proteins.International journal of molecular medicine · 2021Article
- Trials and tribulations of pancreatic cancer immunotherapy.Cancer letters · 2021Review
- The BET family in immunity and disease.Signal transduction and targeted therapy · 2021Review
- Transcriptional Regulation of Cancer Immune Checkpoints: Emerging Strategies for Immunotherapy.Vaccines · 2020Review
Corrections and comments
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Authors and funding
14 authors at 7 institutions in 1 country.
Funding
Abstract
The fibrotic reaction is a characteristic feature of human pancreatic ductal adenocarcinoma (PDAC) tumors. It is associated with activation and proliferation of pancreatic stellate cells (PSCs), which are key regulators of fibrosis in vivo. While there is increasing interest in the regulation of PD-L1 expression in cancer and immune cells, the expression and regulation of PD-L1 in other stromal cells, such as PSCs, has not been fully evaluated. Here we show that PSCs in vitro express higher PD-L1 mRNA and protein levels compared to the levels present in PDAC cells. We show that inhibitors targeting bromodomain and extra-terminal (BET) proteins and BRD4 knockdown decrease interferon-γ (IFN-γ)-induced PD-L1 expression in PSCs. We also show that c-MYC, one of the well-established targets of BET inhibitors, does not mediate IFN-γ-regulated PD-L1 expression in PSCs. Instead we show that interferon regulatory factor 1 (IRF1) mediates IFN-γ-induced PD-L1 expression in PSCs. Finally, while we show that BET inhibitors do not regulate IFN-γ-induced IRF1 expression in PSCs, BET inhibitors decrease binding of IRF1 and BRD4 to the PD-L1 promoter. Together, these results demonstrate the interplay between IRF1 and BRD4 in the regulation of PD-L1 in PSCs.
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Registered trials
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