Scientific article

Osteoblasts remotely supply lung tumors with cancer-promoting SiglecFhigh neutrophils

Published inScience, vol. 358, no. 6367, eaal5081
Publication date2017

Bone marrow-derived myeloid cells can accumulate within tumors and foster cancer outgrowth. Local immune-neoplastic interactions have been intensively investigated, but the contribution of the systemic host environment to tumor growth remains poorly understood. Here, we show in mice and cancer patients (n = 70) that lung adenocarcinomas increase bone stromal activity in the absence of bone metastasis. Animal studies reveal that the cancer-induced bone phenotype involves bone-resident osteocalcin-expressing (Ocn+) osteoblastic cells. These cells promote cancer by remotely supplying a distinct subset of tumor-infiltrating SiglecFhigh neutrophils, which exhibit cancer-promoting properties. Experimentally reducing Ocn+ cell numbers suppresses the neutrophil response and lung tumor outgrowth. These observations posit osteoblasts as remote regulators of lung cancer and identify SiglecFhigh neutrophils as myeloid cell effectors of the osteoblast-driven protumoral response.

  • Adenocarcinoma/pathology
  • Adenocarcinoma of Lung
  • Animals
  • Antigens
  • CD/metabolism
  • Antigens
  • Differentiation
  • Myelomonocytic/metabolism
  • Bone Density
  • Bone Marrow Cells/pathology
  • Bone and Bones/metabolism/pathology
  • Cell Line
  • Tumor
  • Humans
  • Lectins/metabolism
  • Lung Neoplasms/pathology
  • Mice
  • Mice
  • Inbred C57BL
  • Myeloid Cells/pathology
  • Neoplasms
  • Experimental/pathology
  • Neutrophil Infiltration
  • Neutrophils/metabolism/pathology
  • Osteoblasts/pathology
  • Osteocalcin/metabolism
  • Receptor for Advanced Glycation End Products/metabolism
Affiliation Not a UNIGE publication
Citation (ISO format)
ENGBLOM, Camilla et al. Osteoblasts remotely supply lung tumors with cancer-promoting SiglecFhigh neutrophils. In: Science, 2017, vol. 358, n° 6367, p. eaal5081. doi: 10.1126/science.aal5081
Main files (1)
Article (Published version)
ISSN of the journal0036-8075

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