ArticleThe Journal of clinical investigation2022
LC3-associated phagocytosis in bone marrow macrophages suppresses acute myeloid leukemia progression through STING activation.
Article in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 64 citations in OpenAlex.
- Evolving landscape of targeted immunotherapeutic interventions and CAR-T therapy for acute myeloid leukemia.NPJ precision oncology · 2026Review
- Remodeling the tumor immune microenvironment: mechanisms of crosstalk between regulated cell death macrophages.Frontiers in immunology · 2026Review
- cGAS-STING signaling pathway as a therapeutic target in human diseases.Chinese medical journal · 2025Review
- New Insight into Bone Immunity in Marrow Cavity and Cancellous Bone Microenvironments and Their Regulation.Biomedicines · 2025Review
- Dual roles and therapeutic targeting of tumor-associated macrophages in tumor microenvironments.Signal transduction and targeted therapy · 2025Review
- Ferroptosis-mediated immune responses in osteoporosis.Journal of orthopaedic translation · 2025Review
- The rewired immune microenvironment in leukemia.Nature immunology · 2025Review
- Article
- Neutrophil Engulfment in Cancer: Friend or Foe?Cancers · 2025Review
- Iron overload promotes myeloid differentiation of normal hematopoietic stem cells and educates macrophage mediated immunosuppression in acute myeloid leukemia.Frontiers in immunology · 2025Article
- The interplay of mitochondrial dysfunction and altered metabolic pathways in glioblastoma.Contemporary oncology (Poznan, Poland) · 2025Review
- The role of type I interferon signaling in myeloid anti-tumor immunity.Frontiers in immunology · 2025Review
- M1 macrophage-derived exosomes alleviate leukemia by causing mitochondrial dysfunction.Annals of hematology · 2024Article
- Nanoparticles and bone microenvironment: a comprehensive review for malignant bone tumor diagnosis and treatment.Molecular cancer · 2024Review
- Low protein diet protects the liver from Salmonella Typhimurium-mediated injury by modulating the mTOR/autophagy axis in macrophages.Communications biology · 2024Article
- Acute myeloid leukemia-driven IL-3-dependent upregulation of BCL2 in non-malignant hematopoietic stem and progenitor cells increases venetoclax-induced cytopenias.Haematologica · 2024Article
- STING inhibition suppresses microglia-mediated synapses engulfment and alleviates motor functional deficits after stroke.Journal of neuroinflammation · 2024Article
- Macrophage senescence in health and diseases.Acta pharmaceutica Sinica. B · 2024Review
- The KIR2DL family serves as prognostic biomarkers and correlates with immune infiltrates in acute myeloid leukaemia.Journal of cellular and molecular medicine · 2024Article
- Harnessing innate immune pathways for therapeutic advancement in cancer.Signal transduction and targeted therapy · 2024Review
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11 authors at 2 institutions in 1 country.
Funding
Abstract
The bone marrow (BM) microenvironment regulates acute myeloid leukemia (AML) initiation, proliferation, and chemotherapy resistance. Following cancer cell death, a growing body of evidence suggests an important role for remaining apoptotic debris in regulating the immunologic response to and growth of solid tumors. Here, we investigated the role of macrophage LC3-associated phagocytosis (LAP) within the BM microenvironment of AML. Depletion of BM macrophages (BMMs) increased AML growth in vivo. We show that LAP is the predominate method of BMM phagocytosis of dead and dying cells in the AML microenvironment. Targeted inhibition of LAP led to the accumulation of apoptotic cells (ACs) and apoptotic bodies (ABs), resulting in accelerated leukemia growth. Mechanistically, LAP of AML-derived ABs by BMMs resulted in stimulator of IFN genes (STING) pathway activation. We found that AML-derived mitochondrial damage-associated molecular patterns were processed by BMMs via LAP. Moreover, depletion of mitochondrial DNA (mtDNA) in AML-derived ABs showed that it was this mtDNA that was responsible for the induction of STING signaling in BMMs. Phenotypically, we found that STING activation suppressed AML growth through a mechanism related to increased phagocytosis. In summary, we report that macrophage LAP of apoptotic debris in the AML BM microenvironment suppressed tumor growth.
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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.