© 1992 by Oxford University Press
Journal of the National Cancer Institute, Vol. 84, No. 7, 523-527,
April 1992
© 1992 Oxford University Press
Effects of Transforming Growth Factor-
on Human Pulmonary Adenocarcinoma Cell Adhesion, Motility, and Invasion In Vitro
Department of Laboratory Medicine and Pathology and the Biomedical Engineering Center, University of Minnesola Minneapolis
*Correspondence to: Daniel L. Mooradian, Ph.D., Department of Laboratory Medicine and Pathology, Box 609 Mayo Memorial Building, University of Minnesota, 420 Delaware St., S.E., Minneapolis, MN 55455.
Background: Transforming growth factor-
pl (TGF-1), a potent growth modulator produced by a variety of tumor cells, as well as by platelets, has pleiotropic effects on cell-extracellular matrix interactions and may influence tumor cell invasion and metastasis. Purpose: Our purpose was to characterize the effects of TGF-1 on the adhesion, motility, and invasiveness of a metastatic human pulmonary carcinoma (A549 cell line) in vitro. Methods: A549 cells were seeded onto type I collagen gels, and invasion over a 9-day period was measured in the presence or absence of TGF-1 (0.1–10 ng/mL). In addition, cell adhesion to substrata coated with type I collagen (1–100 nM) as well as haptotactic migration through filters coated with type I collagen (100 µg/mL) were measured following a 24-hour treatment with TGF-1 (1–10 ng/mL). Results: TGF-1 stimulated the invasion of A549 cells into type I collagen gels in a dose-dependent manner. Both the number of cells entering the gel and the depth of invasion into the gel were increased. In addition, the effects,of TGF-1 were blocked in a dose-dependent manner by a purified polyclonal IgG against TGF-1 but not by normal rabbit IgG. A549 cell invasion was accompanied by dramatic changes in A549 cell morphology that included the appearance of numerous long pseudo-podia, consistent with a change in the motile behavior of these cells. TGF-1 stimulated by approximately fourfold the haptotactic migration of A549 cells on haptotactic migration of A549 cells on polycarbonate filters coated with type I collagen. The TGF-1-mediated increase in invasion and motility was accompanied by a fourfold increase in A549 cell adhesion to type I collagen. Conclusions: The results suggest that TGF-1 can influence cellular recognition of extracellular matrix components and can modulate cellular adhesion and migration on these components, leading to increased invasive potential. Implications: Given the widespread tissue distribution of TGF-1 and its secretion by a variety of tumor cells as well as by platelets, TGF-1 may be an important autocrineparacrine regulator of the invasive phenotype in vivo. (J Natl Cancer Inst 84: 523–527, 1992)
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