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1 Division of Hematology-Oncology, Department of Pediatrics, and Departments of 2 Pathology and 3 Biochemistry and Molecular Biology, Keck School of Medicine; 4 School of Dentistry, University of Southern California; 5 The Saban Research Institute of Childrens Hospital Los Angeles, Los Angeles, California; and 6 Stem Cell Biology Section, Departments of Medicine and Immunology & Pathology, Washington University, St. Louis, Missouri
Requests for reprints: Yves A. DeClerck, Division of Hematology-Oncology, Childrens Hospital Los Angeles, Los Angeles, CA 90027. Phone: 323-669-2150; Fax: 323-664-9455; E-mail: declerck{at}usc.edu.
The bone is the third most common site of cancer metastasis. To invade the bone, tumor cells produce osteoclast-activating factors that increase bone resorption by osteoclasts. Here we report that human neuroblastoma cells that form osteolytic lesions in vivo do not produce osteoclast-activating factors but rather stimulate osteoclast activity in the presence of human bone marrow mesenchymal stem cells. This alternative pathway of osteoclast activation involves a nonadhesive interaction between neuroblastoma cells and bone marrow mesenchymal stem cells. Stimulated bone marrow mesenchymal stem cells express markedly increased levels of interleukin-6, which is then responsible for osteoclast activation. This report describes a critical role of bone marrow mesenchymal stem cells in bone destruction in cancer.
Key Words: neuroblastoma • bone marrow mesenchymal stem cells • bone invasion • interleukin-6 • osteoclasts
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