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Platelet and osteoclast β3 integrins are critical for bone metastasis
Journal article   Open access   Peer reviewed

Platelet and osteoclast β3 integrins are critical for bone metastasis

Suzanne J Bakewell, Patrick Nestor, Srinivasa Prasad, Michael H Tomasson, Nikki Dowland, Mukund Mehrotra, Robert Scarborough, James Kanter, Keith Abe, David Phillips, …
Proceedings of the National Academy of Sciences - PNAS, Vol.100(24), pp.14205-14210
11/25/2003
DOI: 10.1073/pnas.2234372100
PMCID: PMC283570
PMID: 14612570
url
https://doi.org/10.1073/pnas.2234372100View
Published (Version of record) Open Access

Abstract

Mice with a targeted deletion of β3 integrin were used to examine the process by which tumor cells metastasize and destroy bone. Injection of B16 melanoma cells into the left cardiac ventricle resulted in osteolytic bone metastasis in 74% of β3+/+ mice by 14 days. In contrast, only 4% of β3–/– mice developed bone lesions. Direct intratibial inoculation of tumor resulted in marrow replacement by tumor in β3–/– mice, but no associated trabecular bone resorption as seen inβ3+/+ mice. Bone marrow transplantation studies showed that susceptibility to bone metastasis was conferred by a bone marrow-derived cell. To dissect the roles of osteoclast and platelet β3 integrins in this model of bone metastasis, osteoclast-defective src–/– mice were used. Src-null mice were protected from tumor-associated bone destruction but were not protected from tumor cell metastasis to bone. In contrast, a highly specific platelet aggregation inhibitor of activated αIIbβ3 prevented B16 metastases. These data demonstrate a critical role for platelet αIIbβ3 in tumor entry into bone and suggest a mechanism by which antiplatelet therapy may be beneficial in preventing the metastasis of solid tumors.
Biological Sciences

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