ArticleScientific reports2016
Entinostat up-regulates the CAMP gene encoding LL-37 via activation of STAT3 and HIF-1α transcription factors.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 46 citations in OpenAlex.
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- Update on antimicrobial peptides: key elements inThe Journal of general virology · 2025Review
- Enhancement of innate immunity in gingival epithelial cells by vitamin D and HDAC inhibitors.Frontiers in oral health · 2024Article
- High-Throughput Screening for Epigenetic Compounds That Induce Human β-Defensin 1 Synthesis.Antibiotics (Basel, Switzerland) · 2023Article
- Histone deacetylase (HDAC) inhibitors- based drugs are effective to control Mycobacterium tuberculosis infection and promote the sensibility for rifampicin in MDR strain.Memorias do Instituto Oswaldo Cruz · 2023Article
- Modulation of innate immunity in airway epithelium for host-directed therapy.Frontiers in immunology · 2023Review
- Sprouty1 exerts a preventive effect on the initiation of psoriasis by inhibiting innate immune antimicrobial peptide cathelicidin and immunocytes.Cell proliferation · 2022Article
- Large-Scale Identification of Multiple Classes of Host Defense Peptide-Inducing Compounds for Antimicrobial Therapy.International journal of molecular sciences · 2022Article
- Chasing a Breath of Fresh Air in Cystic Fibrosis (CF): Therapeutic Potential of Selective HDAC6 Inhibitors to Tackle Multiple Pathways in CF Pathophysiology.Journal of medicinal chemistry · 2022Review
- Antimicrobial production by perifollicular dermal preadipocytes is essential to the pathophysiology of acne.Science translational medicine · 2022Article
- High Vitamin D Concentrations Restore the Ability to Express LL37 byBiomolecules · 2022Article
- The Novel Inducer of Innate Immunity HO53 Stimulates Autophagy in Human Airway Epithelial Cells.Journal of innate immunity · 2022Article
- Upregulating Human Cathelicidin Antimicrobial Peptide LL-37 Expression May Prevent Severe COVID-19 Inflammatory Responses and Reduce Microthrombosis.Frontiers in immunology · 2022Review
- HIF-1 mediated activation of antimicrobial peptide LL-37 in type 2 diabetic patients.Journal of molecular medicine (Berlin, Germany) · 2022Article
- Hypoxia and HIF-1 as key regulators of gut microbiota and host interactions.Trends in immunology · 2021Review
- Entinostat augments NK cell functions via epigenetic upregulation of IFIT1-STING-STAT4 pathway.Oncotarget · 2020Article
- A mouse model for vitamin D-induced human cathelicidin antimicrobial peptide gene expression.The Journal of steroid biochemistry and molecular biology · 2020Article
- Host Directed Therapy Against Infection by Boosting Innate Immunity.Frontiers in immunology · 2020Review
- Novel aroylated phenylenediamine compounds enhance antimicrobial defense and maintain airway epithelial barrier integrity.Scientific reports · 2019Article
- Differential Expression of Antimicrobial Peptides in Streptococcus pneumoniae Keratitis and STAT3-Dependent Expression of LL-37 by Streptococcus pneumoniae in Human Corneal Epithelial Cells.Pathogens (Basel, Switzerland) · 2019Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Bacterial resistance against classical antibiotics is a growing problem and the development of new antibiotics is limited. Thus, novel alternatives to antibiotics are warranted. Antimicrobial peptides (AMPs) are effector molecules of innate immunity that can be induced by several compounds, including vitamin D and phenyl-butyrate (PBA). Utilizing a luciferase based assay, we recently discovered that the histone deacetylase inhibitor Entinostat is a potent inducer of the CAMP gene encoding the human cathelicidin LL-37. Here we investigate a mechanism for the induction and also find that Entinostat up-regulates human β-defensin 1. Analysis of the CAMP promoter sequence revealed binding sites for the transcription factors STAT3 and HIF-1α. By using short hairpin RNA and selective inhibitors, we found that both transcription factors are involved in Entinostat-induced expression of LL-37. However, only HIF-1α was found to be recruited to the CAMP promoter, suggesting that Entinostat activates STAT3, which promotes transcription of CAMP by increasing the expression of HIF-1α. Finally, we provide in vivo relevance to our findings by showing that Entinostat-elicited LL-37 expression was impaired in macrophages from a patient with a STAT3-mutation. Combined, our findings support a role for STAT3 and HIF-1α in the regulation of LL-37 expression.
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