Inhibition of epidermal growth factor receptor functions by tyrosine kinase inhibitors in NIH3T3 cells
Open Access
- 17 December 1992
- journal article
- Published by Wiley in FEBS Letters
- Vol. 314 (3) , 289-292
- https://doi.org/10.1016/0014-5793(92)81491-4
Abstract
Epidermal growth factor (EGF) induces transformed phenotypes in EGF receptor‐overexpressing NIH3T3 (ER12) cells. Tyrosine kinase inhibitors such as erbstatin and its stable analogue methyl 2,5‐dihydroxycinnamate inhibited the EGF‐induced phenotypes changes in these cells; while 5′‐O‐methylerbstatin, an inactive analogue, did not. Methyl 2,5‐dihydroxycinnamate inhibited intracellular tyrosine kinase activity in EGF‐treated ER12 cells. Methyl 2,5‐dihydroxycinnamate also delayed the EGF‐induced DNA synthesis from the quiescent phase ER12 cells without showing irreversible cytotoxicity. It inhibited the DNA synthesis most efficiently at the early G1 phase. Thus, tyrosine kinase inhibitors may modify malignant phenotypes in EGF receptor‐overexpressing neoplasms.Keywords
This publication has 12 references indexed in Scilit:
- Induction of morphological change by tyrosine kinase inhibitors in Rous sarcoma virus-transformed rat kidney cellsFEBS Letters, 1991
- [32] Use of erbstatin as protein-tyrosine kinase inhibitorPublished by Elsevier ,1991
- Inhibition of epidermal growth factor‐induced DNA synthesis by tyrosine kinase inhibitorsFEBS Letters, 1990
- PDGF induction of tyrosine phosphorylation of GTPase activating proteinNature, 1989
- Phospholipase C-γ is a substrate for the PDGF and EGF receptor protein-tyrosine kinases in vivo and in vitroCell, 1989
- PDGF-dependent tyrosine phosphorylation stimulates production of novel polyphosphoinositides in intact cellsCell, 1989
- Epidermal-Growth-Factor-Dependent Transformation by a Human EGF Receptor Proto-OncogeneScience, 1987
- Overexpression of the human EGF receptor confers an EGF-dependent transformed phenotype to NIH 3T3 cellsCell, 1987
- Increased expression of the epidermal growth factor receptor gene in malignant gliomas is invariably associated with gene amplification.Proceedings of the National Academy of Sciences, 1987
- Amplification, enhanced expression and possible rearrangement of EGF receptor gene in primary human brain tumours of glial originNature, 1985