Fibronectin/laminin and their receptors in aberrant growth control in FR3T3 cells transformed by ha‐ras oncogene and epidermal growth factor gene

Abstract

FR3T3 cells transfected with either the Ha-ras oncogene or the epidermal-growth-factor (EGF) gene demonstrate the transformed phenotype as indicated by in vitro and in vivo criteria. We have examined non-transformed FR3T3 cells as well as Ha-ras-oncogene-transformed and EGF-gene-transformed cells for expression of cell surface fibronectin and cell surface laminin. Fibronectin was absent from the surface of the Ha-ras-oncogene-transformed cells but present on both the EGF-gene-transformed cells and the non-transformed FR3T3 cells. Laminin was present on the cell surface in all 3 lines. The lack of surface fibronectin on the Ha-ras-oncogene-transformed cells was associated with reduced fibronectin production as indicated by immunoblotting of whole cell extracts and by ELISA. Concomitantly, there was a significant reduction of fibronectin binding by the Ha-ras-oncogene-transformed cells was compared to their EGF-gene-transformed and non-transformed counterparts. The Ha-ras-oncogene-transformed cells demonstrated reduced cell-substrate adhesiveness relative to the other two cell lines, as indicated by rates of attachment and spreading on plastic culture dishes in the presence of bovine serum albumin. They also demonstrated reduced adhesiveness in response to fibronectin but not laminin. Taken together, our results suggest that aberrant expression of fibronectin/fibronectin receptors is associated with Ha-ras-oncogene-induced transformation. In contrast, transformation by the EGF gene does not appear to involve aberrant expression of fibronectin/fibronectin receptors.