ArticleJournal of cellular biochemistry2014
Osteoblasts protect AML cells from SDF-1-induced apoptosis.
Article in Journal of cellular biochemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 56 citations in OpenAlex.
- The Role of the Bone Marrow Microenvironment in the Pathogenesis of Acute Myeloid Leukemia.Biomedicines · 2026Review
- Article
- Protein serine/threonine phosphatases in tumor microenvironment: a vital player and a promising therapeutic target.Theranostics · 2025Review
- CXCR4 as a therapeutic target in acute myeloid leukemia.Leukemia · 2024Review
- Fabrication of a three-dimensional bone marrow niche-like acute myeloid Leukemia disease model by an automated and controlled process using a robotic multicellular bioprinting system.Biomaterials research · 2023Article
- AML alters bone marrow stromal cell osteogenic commitment via Notch signaling.Frontiers in immunology · 2023Article
- Article
- Osteoblast Lineage Support of Hematopoiesis in Health and Disease.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022Review
- Deciphering the Therapeutic Resistance in Acute Myeloid Leukemia.International journal of molecular sciences · 2020Review
- Location First: Targeting Acute Myeloid Leukemia Within Its Niche.Journal of clinical medicine · 2020Review
- Highly multiplexed proteomic assessment of human bone marrow in acute myeloid leukemia.Blood advances · 2020Article
- S100 Proteins in Acute Myeloid Leukemia.Neoplasia (New York, N.Y.) · 2018Review
- Osteogenic niche in the regulation of normal hematopoiesis and leukemogenesis.Haematologica · 2018Review
- Tissue-Nonspecific Alkaline Phosphatase Is Required for MC3T3 Osteoblast-Mediated Protection of Acute Myeloid Leukemia Cells from Apoptosis.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Cytokines increase engraftment of human acute myeloid leukemia cells in immunocompromised mice but not engraftment of human myelodysplastic syndrome cells.Haematologica · 2018Article
- Endosteal vessel integrity: a new therapeutic goal in acute myeloid leukemia?Stem cell investigation · 2018Article
- Histone Deacetylase 3 Deletion in Mesenchymal Progenitor Cells Hinders Long Bone Development.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2017Article
- Histone deacetylase inhibitors reduce differentiating osteoblast-mediated protection of acute myeloid leukemia cells from cytarabine.Oncotarget · 2017Article
- The role and clinical implications of the endosteal niche and osteoblasts in regulating leukemia.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2017Review
- Reciprocal Interactions of Leukemic Cells with Bone Marrow Stromal Cells Promote Enrichment of Leukemic Stem Cell Compartments in Response to Curcumin and DaunorubicinAsian Pacific journal of cancer prevention : APJCP · 2017Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
The bone marrow provides a protective environment for acute myeloid leukemia (AML) cells that often allows leukemic stem cells to survive standard chemotherapeutic regimens. Targeting these leukemic stem cells within the bone marrow is critical for preventing relapse. We recently demonstrated that SDF-1, a chemokine abundant in the bone marrow, induces apoptosis in AML cell lines and in patient samples expressing high levels of its receptor, CXCR4. Here we show that a subset of osteoblast lineage cells within the bone marrow can protect AML cells from undergoing apoptosis in response to the SDF-1 naturally present in that location. In co-culture systems, osteoblasts at various stages of differentiation protected AML cell lines and patient isolates from SDF-1-induced apoptosis. The differentiation of the osteoblast cell lines, MC3T3 and W-20-17, mediated this protection via a cell contact-independent mechanism. In contrast, bone marrow-derived mesenchymal cells, the precursors of osteoblasts, induced apoptosis in AML cells via a CXCR4-dependent mechanism and failed to protect AML cells from exogenously added SDF-1. These results indicate that osteoblasts in the process of differentiation potently inhibit the SDF-1-driven apoptotic pathway of CXCR4-expressing AML cells residing in the bone marrow. Drugs targeting this protective mechanism could potentially provide a new approach to treating AML by enhancing the SDF-1-induced apoptosis of AML cells residing within the bone marrow 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.