Role of TGF-beta in EGF-induced transformation of NRK cells is sustaining high-level EGF-signaling |
| |
Authors: | Kizaka-Kondoh S Akiyama N Okayama H |
| |
Affiliation: | Department of Molecular Oncology, Kyoto University Graduate School of Medicine, Yoshida-Konoe-cho, Sakyo-ku, Kyoto, Japan. skondoh@virus1.virus.kyoto-u.ac.jp |
| |
Abstract: | We have been isolating and analyzing NRK cell mutants, which fail to transform by epidermal growth factor (EGF) and transforming growth factor (TGF)-beta. One such mutant, R14, can respond to the growth inhibitory signal of TGF-beta to the same extent as parental NRK but fail to respond to the growth stimulatory signal of EGF. This mutant has a defect in EGF receptor (EGFR) expression. When R14 mutant expressed a high level of EGFR, however, EGF not only induced proliferation in this mutant but also induced transformation without the aid of TGF-beta. These findings suggest that the major role of TGF-beta in this transformation system should be to counteract the ligand-dependent down-regulation of EGFR, thereby sustaining high-level EGF-signaling. |
| |
Keywords: | |
本文献已被 PubMed 等数据库收录! |
|