||Introduction of a Ha-ras Oncogene into Rat Liver Epithelial Cells and Parenchymal Hepatocytes Confers Resistance to the Growth Inhibitory Effects of TGF-Beta.
Houck, K. A. ;
Michalopoulos, G. K. ;
Strom, S. C. ;
||Duke Univ. Medical Center, Durham, NC. Dept. of Pathology. ;Virginia Commonwealth Univ., Richmond.;Health Effects Research Lab., Research Triangle Park, NC.
Deoxyribonucleic acids ;
Transforming growth factors ;
Ras genes ;
||Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy.
||Growth of rat liver epithelial cells (RLEC) and primary cultures of parenchymal hepatocytes is potently inhibited by TGF-Beta. Transfection of a mutated Ha-ras oncogene, but not a human c-myc oncogene, into RLEC resulted in cell lines resistant to growth inhibition by TGF-Beta under anchorage-dependent conditions. Infection of primary rat hepatocyte cultures with v-Ha-ras yielded a cell line likewise insensitive to inhibition by TGF-Beta. Binding of (125I)TGF-Beta to Ha-ras-transfected RLEC was reduced relative to control or c-myc-transfected cells. These data suggest that activation of a Ha-ras oncogene in epithelial cells may result in escape from negative growth control and hence be a critical step during carcinogenesis. (Copyright (c) 1989 The MacMillan Press Ltd.)
||Pub. in Oncogene 4, p19-25 1989. Prepared in cooperation with Virginia Commonwealth Univ., Richmond. Sponsored by Health Effects Research Lab., Research Triangle Park, NC.
|NTIS Title Notes
||Reprint: Introduction of a Ha-ras Oncogene into Rat Liver Epithelial Cells and Parenchymal Hepatocytes Confers Resistance to the Growth Inhibitory Effects of TGF-Beta.
||PC A02/MF A01