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Regulation of human colon‐carcinoma cell adhesion to extracellular matrix by transforming growth factor β1

The regulatory effect of transforming growth factor β1 (TGF‐β1) on the adhesion of human colon‐carcinoma cells to the extracellular matrix (ECM) was investigated. ECMs used in this study included tissue‐culture wells coated with fibronectin, laminin, collagen and BSA, as well as plastic wells. Three phenotypically different human colon‐carcinoma cell lines (Moser, HCT116, and KM 12SM) were used. The Moser cell line is moderately differentiated and, in terms of the diversity of responses elicited by TGF‐β1, is the human colon‐carcinoma cell line most responsive to TCP‐β1 as reported to date. By comparison, the undifferentiated HCT116 and the highly meta‐ static KM 12SM cells are unresponsive to this growth factor. We showed that TGF‐β1 regulated the adhesion responses of all 3 cell lines. However, the response profiles as well as the endogenous adhesive properties of each cell line were quite different from those of the others. Endogenous Arg‐Gly‐Asp(RGD)‐related receptors were present on the HCT 116 but not on the other cells. The observed regulatory effect of TGF‐β1 was contingent on the cell line, the type of ECM, and the growth‐factor treatment protocol used. When cells were treated with TGF‐PI for 16 hr prior to exposure to ECM in a 4‐hr adhesion assay, a significant increase in adhesion to fibronectin and collagen was observed for the Moser cells. For the identical experimental protocol, the KM 12SM cells responded by increas‐ ing adhesion to fibronectin, while the HCT 116 cells responded by decreasing adhesion to collagen. Kinetic analyses of TGF‐p I treatment showed that increased adhesion response to laminin was induced in the Moser cells after 2 hr of growth‐factor treatment. This response declined rapidly upon further exposure of the cells to TGF‐β1. Simultaneous exposure of cells to both TGF‐β1 and ECM negated the adhesion responses described above. The up‐modulation of adhesion to fibronectin, laminin and collagen by TGF‐β1 was mediated through RGD‐related integrin receptors. RGD‐containing peptides effectively blocked the enhanced adhesion responses induced by TGF‐β1.