Main Title |
Introduction of a Ha-ras Oncogene into Rat Liver Epithelial Cells and Parenchymal Hepatocytes Confers Resistance to the Growth Inhibitory Effects of TGF-Beta. |
Author |
Houck, K. A. ;
Michalopoulos, G. K. ;
Strom, S. C. ;
|
CORP Author |
Duke Univ. Medical Center, Durham, NC. Dept. of Pathology. ;Virginia Commonwealth Univ., Richmond.;Health Effects Research Lab., Research Triangle Park, NC. |
Publisher |
c1989 |
Year Published |
1989 |
Report Number |
EPA-R-814344; EPA/600/J-89/203; |
Stock Number |
PB90-147794 |
Additional Subjects |
Liver ;
Epithelium ;
Cells(Biology) ;
Deoxyribonucleic acids ;
Reprints ;
Transforming growth factors ;
Transfection ;
Oncogenes ;
Protooncogenes ;
Autoradiography ;
Ras genes ;
Southern immunoblotting
|
Holdings |
Library |
Call Number |
Additional Info |
Location |
Last Modified |
Checkout Status |
NTIS |
PB90-147794 |
Some EPA libraries have a fiche copy filed under the call number shown. |
|
07/26/2022 |
|
Collation |
9p |
Abstract |
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.) |