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Macrophage Colony-stimulating Factor (CSF-1) Enhances Invasiveness in CSF-1 Receptor-positive Carcinoma Cell Lines¹

Pulmonary and Critical Care Section, New England Deaconess Hospital, Harvard Medical School, Boston, Massachusetts 02215 [A. E. F., N. D.]; Department of Rheumatology and Immunology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts [A. B., H. G. R.]; and Department of Therapeutic Radiology, Yale University School of Medicine, New Haven, Connecticut [B. M. K.]

We have identified two lung carcinoma cell lines, A549 and Calu-1, expressing low levels of the macrophage colony-stimulating factor (CSF-1) receptor (CSF-1R), encoded by the c-fms oncogene. The effect of CSF-1 on the invasive potential of these CSF-1R-positive tumor cell lines and on two other CSF-1R-bearing cell lines, the BT-20 breast carcinoma cell line and the CSF-1 growth-dependent murine macrophage cell line BAC1.2F5, was examined using a human amnionic basement membrane invasion model. Culture of A549, Calu-1, and BAC1.2F5 cells with CSF-1 (250 ng/ml) resulted in a maximal 12-, 5-, and 12-fold enhancement of invasion, respectively, compared to control cells cultured in medium alone. Larger concentrations of CSF-1 (750 ng/ml) reduced A549 and Calu-1 invasiveness compared to the effect of the 250-ng/ml dose. Maximal enhancement in invasion of A549 and Calu-1 cells occurred after a 24- and 48-h exposure to CSF-1, respectively. CSF-1 increased invasiveness 6-fold in BT-20 cells induced by glucocorticoids to express high levels of CSF-1R, in comparison to control cells not exposed to glucocorticoids or CSF-1. In contrast, CSF-1 had no effect on invasion in the CSF-1R-negative MCF-7 cell line. Culture of A549 and Calu-1 cells with other cytokines and growth factors including GM-CSF (500 units/ml), IL-3 (1 ng/ml), interferon- (500 units/ml), and tumor necrosis factor (50 units/ml) had no significant effect on invasiveness. Thus, CSF-1 increases invasiveness in CSF-1R-positive tumor cell lines, suggesting a role in enhancing the metastatic potential of tumor cells expressing the CSF-1R.

¹ This work was supported by NIH Grants AI22532, CA47292, and NICHD-28095, American Cancer Society Grant PDT433, and Bristol-Myers Grant R100069.

² To whom requests for reprints should be addressed, at Pulmonary and Critical Care Section, St. Joseph Hospital, 2900 N. Lake Shore Drive, Chicago, IL 60657.

Received 12/ 3/91. Accepted 4/22/92.

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