ArticleCell death & disease2021
BMI1 regulates multiple myeloma-associated macrophage's pro-myeloma functions.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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
23 citing papers in PubMed, 24 citations in OpenAlex.
- Review
- Targeting MYC-Driven Cancers: From Oncogenic Addiction to Therapeutic Vulnerability.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026Review
- Genetic Variants of BMI1 (rs1042059 and rs11591377) and Their Potential Role in Leukemia Susceptibility: A Narrative Review.Health science reports · 2026Article
- Multi-omics Approaches to CCAAT/Enhancer-Binding Protein Beta in Oral Squamous Cell Carcinoma: Crosstalk Between Tumor Cells and Tumor-Associated Macrophages Driving Disease Progression.Current cancer drug targets · 2026Article
- Bmi1 regulates neural differentiation of mesenchymal stem cells through the Wnt3a‑RhoA signaling pathway to repair ischemic brain injury in rats.International journal of molecular medicine · 2025Article
- Review
- Progress and prospects of the combination of BMI1-targeted therapy and immunotherapy in cervical cancer.American journal of cancer research · 2025Review
- Interactions between hedgehog signaling pathway and the complex tumor microenvironment in breast cancer: current knowledge and therapeutic promises.Cell communication and signaling : CCS · 2024Review
- Mesenchymal stem cells-macrophages crosstalk and myeloid malignancy.Frontiers in immunology · 2024Review
- High NEK2 expression in myeloid progenitors suppresses T cell immunity in multiple myeloma.Cell reports. Medicine · 2023Article
- Tumor-Associated Macrophages in Multiple Myeloma: Key Role in Disease Biology and Potential Therapeutic Implications.Current oncology (Toronto, Ont.) · 2023Review
- Cell-derived nanovesicle-mediated drug delivery to the brain: Principles and strategies for vesicle engineering.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Review
- Ectopic CH60 mediates HAPLN1-induced cell survival signaling in multiple myeloma.Life science alliance · 2023Article
- Bmi-1: A master regulator of head and neck cancer stemness.Frontiers in oral health · 2023Review
- The emerging roles of Hedgehog signaling in tumor immune microenvironment.Frontiers in oncology · 2023Review
- Molecular Crosstalk between Chromatin Remodeling and Tumor Microenvironment in Multiple Myeloma.Current oncology (Toronto, Ont.) · 2022Review
- Tumor-Associated Macrophages and Related Myelomonocytic Cells in the Tumor Microenvironment of Multiple Myeloma.Cancers · 2022Review
- The Crucial Roles of Bmi-1 in Cancer: Implications in Pathogenesis, Metastasis, Drug Resistance, and Targeted Therapies.International journal of molecular sciences · 2022Review
- Extracellular vesicle proteomic analysis leads to the discovery of HDGF as a new factor in multiple myeloma biology.Blood advances · 2022Article
- Tumor-associated macrophages in multiple myeloma: advances in biology and therapy.Journal for immunotherapy of cancer · 2022Review
Corrections and comments
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Authors and funding
22 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple myeloma (MM) is an aggressive malignancy characterized by terminally differentiated plasma cells accumulation in the bone marrow (BM). MM BM exhibits elevated MΦs (macrophages) numbers relative to healthy BM. Current evidence indicates that MM-MΦs (MM-associated macrophages) have pro-myeloma functions, and BM MM-MΦs numbers negatively correlate with patient survival. Here, we found that BMI1, a polycomb-group protein, modulates the pro-myeloma functions of MM-MΦs, which expressed higher BMI1 levels relative to normal MΦs. In the MM tumor microenvironment, hedgehog signaling in MΦs was activated by MM-derived sonic hedgehog, and BMI1 transcription subsequently activated by c-Myc. Relative to wild-type MM-MΦs, BMI1-KO (BMI1 knockout) MM-MΦs from BM cells of BMI1-KO mice exhibited reduced proliferation and suppressed expression of angiogenic factors. Additionally, BMI1-KO MM-MΦs lost their ability to protect MM cells from chemotherapy-induced cell death. In vivo analysis showed that relative to wild-type MM-MΦs, BMI1-KO MM-MΦs lost their pro-myeloma effects. Together, our data show that BMI1 mediates the pro-myeloma functions of MM-MΦs.
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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.