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Transactivation of epidermal growth factor receptor by insulin‐like growth factor 1 requires basal hydrogen peroxide
Author(s) -
Zhou Qiong,
Meng Dan,
Yan Bing,
Jiang Bing-Hua,
Fang Jing
Publication year - 2006
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/j.febslet.2006.08.068
Subject(s) - du145 , epidermal growth factor receptor , transactivation , growth factor receptor inhibitor , insulin like growth factor , growth factor , epidermal growth factor , mapk/erk pathway , cancer research , growth factor receptor , tgf alpha , chemistry , endocrinology , egfr inhibitors , medicine , biology , microbiology and biotechnology , prostate cancer , receptor , phosphorylation , signal transduction , cancer , biochemistry , transcription factor , lncap , gene
Insulin‐like growth factor (IGF‐1) plays an important role in prostate cancer development. Recent studies suggest that IGF‐1 has mitogenic action through epidermal growth factor receptor (EGFR). However, the mechanism remains largely unknown. Here, we demonstrated in prostate cancer DU145 cells that IGF‐1 induced EGFR transactivation, leading to ERK activation. Matrix metalloproteinase‐mediated shedding of heparin‐binding EGF is involved in this process. Antioxidants and catalase inhibited IGF‐1‐stimulated EGFR phosphorylation, indicating that H 2 O 2 is required for EGFR activation. However, exogenous H 2 O 2 did not activate EGFR or IGF‐1R in DU145 cells. IGF‐1 did not induced production of H 2 O 2 in DU145 cells. Our results suggest that transactivation of EGFR by IGF‐1 requires basal intracellular H 2 O 2 in DU145 cells.