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Osteoblasts protect AML cells from SDF-1-induced apoptosis.

Kimberly N Kremer, Amel Dudakovic, Meghan E McGee-Lawrence

    Journal of Cellular Biochemistry
    |May 23, 2014
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    Summary

    Osteoblasts protect acute myeloid leukemia (AML) cells from apoptosis in the bone marrow microenvironment. Targeting this protective mechanism may enhance AML treatment by promoting leukemic cell death.

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    Area of Science:

    • Hematology
    • Cancer Biology
    • Stem Cell Biology

    Background:

    • Acute myeloid leukemia (AML) stem cells survive chemotherapy within the protective bone marrow niche.
    • Stromal cell-derived factor-1 (SDF-1) induces apoptosis in AML cells expressing CXCR4.
    • Targeting leukemic stem cells in the bone marrow is crucial for preventing AML relapse.

    Purpose of the Study:

    • To investigate the role of osteoblast lineage cells in protecting AML cells from apoptosis within the bone marrow.
    • To elucidate the mechanism by which osteoblasts mediate protection against SDF-1-induced apoptosis in AML cells.

    Main Methods:

    • Co-culture systems using AML cell lines and patient isolates with osteoblast cell lines (MC3T3, W-20-17) and bone marrow-derived mesenchymal cells.
    • Assessment of AML cell apoptosis in response to SDF-1 and co-culture conditions.
    • Investigation of cell contact-dependent versus independent mechanisms of protection.
    • Evaluation of CXCR4 dependency in AML cell apoptosis.

    Main Results:

    • Osteoblasts, at various differentiation stages, protected AML cells from SDF-1-induced apoptosis via a cell contact-independent mechanism.
    • Bone marrow-derived mesenchymal cells induced AML cell apoptosis via a CXCR4-dependent pathway and did not protect against exogenous SDF-1.
    • Differentiating osteoblasts inhibit the SDF-1-driven apoptotic pathway in CXCR4-expressing AML cells within the bone marrow.

    Conclusions:

    • Osteoblasts within the bone marrow microenvironment actively protect AML cells from apoptosis.
    • This osteoblast-mediated protection inhibits the SDF-1/CXCR4 apoptotic signaling pathway in AML cells.
    • Targeting this osteoblast-AML cell interaction presents a potential therapeutic strategy to enhance AML treatment efficacy.