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A more recent version of this article appeared on May 1, 2003
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Submitted on July 3, 2002
Revised on November 25, 2002
Accepted on January 16, 2003
1 Division of Hormone-Dependent Tumor Biology, The Albert Einstein Comprehensive Cancer Center; and Department of Medicine, Albert Einstein College of Medicine, Bronx, New York, 10461, USA
2 Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, New York, 10461, USA
3 Department of Anatomy and Structural Biology, Albert Einstein College of Medicine, Bronx, New York, 10461, USA
4 Center for Oncology and Cell Biology, North Shore-Long Island Jewish Research Institute, NY 11030
5 Department of Oncology, Lombardi Cancer Center, Georgetown University, Washington, DC 20007
* Corresponding author. E-mail address: pestell{at}georgetown.edu.
The cyclin D1 gene encodes the regulatory subunit of a holoenzyme that phosphorylates and inactivates the retinoblastoma protein, pRB, thereby promoting cell-cycle progression. Cyclin D1 is overexpressed in hematopoetic and epithelial malignancies correlating with poor prognosis and metastasis in several cancer types. As 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 (BMM). Cyclin D1 deficiency increased focal complex formation at the site of substratum contact, 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-/- BMM 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.
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