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Vol. 14, Issue 5, 2005-2015, May 2003
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Division of Hormone-dependent Tumor Biology, The Albert Einstein Comprehensive Cancer Center, Bronx, New York 10461;
Departments of Medicine,
Developmental and Molecular Biology, and ||
Anatomy and Structural Biology, Albert Einstein College of Medicine, Bronx, New York, 10461; and
¶
Center for Oncology and Cell Biology, North Shore-Long Island Jewish Research Institute, New York, New York 11030;
#Department of Oncology, Lombardi Cancer Center, Georgetown University,
Washington, DC 20007
Submitted July 3, 2002;
Revised November 25, 2002;
Accepted January 16, 2003
Monitoring Editor: Pamela A. Silver
The cyclin D1 gene encodes the regulatory subunit of a holoenzyme that phosphorylates and inactivates the retinoblastoma protein, thereby promoting cell-cycle progression. Cyclin D1 is overexpressed in hematopoetic and epithelial malignancies correlating with poor prognosis and metastasis in several cancer types. Because tumor-associated macrophages have been shown to enhance malignant progression and metastasis, and cyclin D1-deficient mice are resistant to oncogene-induced malignancies, we investigated the function of cyclin D1-/- bone marrow-derived macrophages. Cyclin D1 deficiency increased focal complex formation at the site of substratum contact, and enhanced macrophage adhesion, yielding a flattened, circular morphology with reduced membrane ruffles. Migration in response to wounding, cytokine-mediated chemotaxis, and transendothelial cell migration of cyclin D1-/- bone marrow-derived macrophages were all substantially reduced. Thus, apart from proliferative and possible motility defects in the tumor cells themselves, the reduced motility and invasiveness of cyclin D1-/- tumor-associated macrophages may contribute to the tumor resistance of these mice.
On line version of this article contains video material. Online version is
available at
www.molbiolcell.org.
* These authors contributed equally to this work.
# Corresponding author. E-mail address: pestell{at}georgetown.edu.
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