ArticleJCI insight2019
MiR-16 regulates crosstalk in NF-κB tolerogenic inflammatory signaling between myeloma cells and bone marrow macrophages.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
35 citing papers in PubMed, 41 citations in OpenAlex.
- Extracellular Vesicles as Master Regulators of Immune Modulation in Multiple Myeloma.International journal of molecular sciences · 2026Review
- The Role of MicroRNAs Carried by Extracellular Vesicles in Tumorigenesis Through Reprogramming the Mitochondrial Information Processing System.International journal of molecular sciences · 2026Review
- miRNA Sequencing and Differential Analysis of Testes from 1-Year-Old and 3-Year-Old Kazakh Horses.Biology · 2026Article
- RNA-Based Therapeutic Strategies in Multiple Myeloma: From Molecular Targets to Delivery and Clinical Translation.International journal of molecular sciences · 2026Review
- Circulating extracellular vesicle-microRNAs (EV-miRNAs) in leukemias and related disorders.Frontiers in medicine · 2026Review
- Extracellular vesicles in the immune regulation of hematological malignancies: mechanisms, prognostic significance, and therapeutic opportunities.Frontiers in cell and developmental biology · 2026Review
- Extracellular vesicles in multiple myeloma: pathogenesis and therapeutic application.The FEBS journal · 2025Review
- A Novel Role for Coilin in Vertebrate Innate Immunity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Proteasome inhibition enhances oncolytic reovirus therapy in multiple myeloma independently of its direct cytotoxic effects.Journal of hematology & oncology · 2025Article
- Article
- NF-κB: Governing Macrophages in Cancer.Genes · 2024Review
- Recent Progress of Exosomes in Hematological Malignancies: Pathogenesis, Diagnosis, and Therapeutic Strategies.International journal of nanomedicine · 2024Review
- d-lactate modulates M2 tumor-associated macrophages and remodels immunosuppressive tumor microenvironment for hepatocellular carcinoma.Science advances · 2023Article
- A Data-Mining Approach to Identify NF-kB-Responsive microRNAs in Tissues Involved in Inflammatory Processes: Potential Relevance in Age-Related Diseases.International journal of molecular sciences · 2023Article
- Extracellular vesicles in hematological malignancies: EV-dence for reshaping the tumoral microenvironment.Frontiers in immunology · 2023Review
- Review
- Distinct non-coding RNA cargo of extracellular vesicles from M1 and M2 human primary macrophages.Journal of extracellular vesicles · 2022Article
- Extracellular Vesicles in Multiple Myeloma-Cracking the Code to a Better Understanding of the Disease.Cancers · 2022Review
- Phosphoinositide 3-kinase/Akt and its related signaling pathways in the regulation of tumor-associated macrophages polarization.Molecular and cellular biochemistry · 2022Review
- Emerging roles of extracellular vesicles in normal and malignant hematopoiesis.The Journal of clinical investigation · 2022Review
Corrections and comments
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Authors and funding
21 authors at 7 institutions in 2 countries.
Funding
Abstract
High levels of circulating miR-16 in the serum of multiple myeloma (MM) patients are independently associated with longer survival. Although the tumor suppressor function of intracellular miR-16 in MM plasma cells (PCs) has been elucidated, its extracellular role in maintaining a nonsupportive cancer microenvironment has not been fully explored. Here, we show that miR-16 is abundantly released by MM cells through extracellular vesicles (EVs) and that differences in its intracellular expression as associated with chromosome 13 deletion (Del13) are correlated to extracellular miR-16 levels. We also demonstrate that EVs isolated from MM patients and from the conditioned media of MM-PCs carrying Del13 more strongly differentiate circulating monocytes to M2-tumor supportive macrophages (TAMs), compared with MM-PCs without this chromosomal aberration. Mechanistically, our data show that miR-16 directly targets the IKKα/β complex of the NF-κB canonical pathway, which is critical not only in supporting MM cell growth, but also in polarizing macrophages toward an M2 phenotype. By using a miR-15a-16-1-KO mouse model, we found that loss of the miR-16 cluster supports polarization to M2 macrophages. Finally, we demonstrate the therapeutic benefit of miR-16 overexpression in potentiating the anti-MM activity by a proteasome inhibitor in the presence of MM-resident bone marrow TAM.
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Registered trials
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.