ArticleLeukemia2020
Targeting histone deacetylase 3 (HDAC3) in the bone marrow microenvironment inhibits multiple myeloma proliferation by modulating exosomes and IL-6 trans-signaling.
Article in Leukemia, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 74 citations in OpenAlex.
- Research progress on lysine acetylation (Review).International journal of molecular medicine · 2026Review
- Review
- Synergistic antitumor effects of 5-fluorouracil and vorinostat in preclinical models of pheochromocytomas and paragangliomas.Endocrine · 2026Article
- Transcription factor, E4BP4, inhibits autophagy and apoptosis in multiple myeloma and promotes the HDAC3-mediated suppression of the Beclin1 promoter to reduce dexamethasone sensitivity.Journal of translational medicine · 2026Article
- Extracellular vesicles in multiple myeloma-bone marrow niche crosstalk: from cellular dialogue to clinical perspectives.Journal of translational medicine · 2025Review
- Elevating cytosolic NADPH metabolism in endothelial cells ameliorates vascular aging.Nature communications · 2025Article
- Extracellular vesicles in multiple myeloma: pathogenesis and therapeutic application.The FEBS journal · 2025Review
- Epigenetic isoforms (DNMT3A/3B and HDAC3/7) potential predictors of endothelial dysfunction and subclinical atherosclerosis.Molecular biology reports · 2025Review
- Therapeutically Harnessing Tumor Cell-Derived Extracellular Vesicles for Multiple Myeloma: Recent Advances and Future Perspectives.Pharmaceutics · 2024Review
- TGF-β: an active participant in the immune and metabolic microenvironment of multiple myeloma : TGF-β in the microenvironment of multiple myeloma.Annals of hematology · 2024Review
- Targeting histone deacetylase 1 (HDAC1) in the bone marrow stromal cells revers imatinib resistance by modulating IL-6 in Ph + acute lymphoblastic leukemia.Annals of hematology · 2024Article
- HDAC1/2 and HDAC3 play distinct roles in controlling adult Meibomian gland homeostasis.The ocular surface · 2024Article
- Fusion with ARRDC1 or CD63: A Strategy to Enhance p53 Loading into Extracellular Vesicles for Tumor Suppression.Biomolecules · 2024Article
- Targeted therapy for multiple myeloma: an overview on CD138-based strategies.Frontiers in oncology · 2024Review
- Simultaneously Targeting Two Coupled Signalling Molecules in the Mesenchymal Stem Cell Support Efficiently Sensitises the Multiple Myeloma Cell Line H929 to Bortezomib.International journal of molecular sciences · 2023Article
- Entinostat-Bortezomib Hybrids against Multiple Myeloma.Molecules (Basel, Switzerland) · 2023Article
- Dissecting molecular mechanisms of immune microenvironment dysfunction in multiple myeloma and precursor conditions.Journal of cancer metastasis and treatment · 2023Article
- Review
- Proteasome Inhibitors Silence Oncogenes in Multiple Myeloma through Localized Histone Deacetylase 3 (HDAC3) Stabilization and Chromatin Condensation.Cancer research communications · 2022Article
- Exosome biogenesis: machinery, regulation, and therapeutic implications in cancer.Molecular cancer · 2022Review
Corrections and comments
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Authors and funding
21 authors at 8 institutions in 4 countries.
Funding
Abstract
Multiple myeloma (MM) is an incurable cancer that derives pro-survival/proliferative signals from the bone marrow (BM) niche. Novel agents targeting not only cancer cells, but also the BM-niche have shown the greatest activity in MM. Histone deacetylases (HDACs) are therapeutic targets in MM and we previously showed that HDAC3 inhibition decreases MM proliferation both alone and in co-culture with bone marrow stromal cells (BMSC). In this study, we investigate the effects of HDAC3 targeting in BMSCs. Using both BMSC lines as well as patient-derived BMSCs, we show that HDAC3 expression in BMSCs can be induced by co-culture with MM cells. Knock-out (KO), knock-down (KD), and pharmacologic inhibition of HDAC3 in BMSCs results in decreased MM cell proliferation; including in autologous cultures of patient MM cells with BMSCs. We identified both quantitative and qualitative changes in exosomes and exosomal miRNA, as well as inhibition of IL-6 trans-signaling, as molecular mechanisms mediating anti-MM activity. Furthermore, we show that HDAC3-KD in BM endothelial cells decreases neoangiogenesis, consistent with a broad effect of HDAC3 targeting in the BM-niche. Our results therefore support the clinical development of HDAC3 inhibitors based not only on their direct anti-MM effects, but also their modulation of the BM microenvironment.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.