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Inhibition of epidermal growth factor receptor functions by tyrosine kinase inhibitors in NIH3T3 cells
Author(s) -
Umezawa Kazuo,
Sugata Daiji,
Yamashita Katsuyuki,
Johtoh Noriko,
Shibuya Masabumi
Publication year - 1992
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(92)81491-4
Subject(s) - tyrosine kinase , epidermal growth factor , receptor tyrosine kinase , tropomyosin receptor kinase c , dna synthesis , ror1 , platelet derived growth factor receptor , biology , microbiology and biotechnology , tyrosine , intracellular , proto oncogene tyrosine protein kinase src , chemistry , receptor , biochemistry , kinase , growth factor , dna
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 G 1 phase. Thus, tyrosine kinase inhibitors may modify malignant phenotypes in EGF receptor‐overexpressing neoplasms.