The Phosphatidylinositol-3 kinase Pathway Is Not Essential for Insulin-like Growth Factor I Receptor-mediated Clonogenic Radioresistance
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概要
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The insulin-like growth factor I receptor (IGF-IR) is known to induce clonogenic radioresistance in cells following ionizing irradiation. To explore the downstream signaling pathways, we focused on the phosphatidylinositol-3 kinase (PI3-K) pathway, which is thought to be the primary cell survival signal originating from the receptor. For this purpose, R- cells deficient in the endogenous IGF-IR were used as a recipient of the human IGF-IR with or without mutations at potential PI3-K activation sites: NPXY^<950> and Y^<1316>XXM. Mutants with double mutation at Y950/Y1316 exhibited not abrogated, but reduced activation of IRS-1, PI3-K, and Akt upon IGF-I stimulation. However, the mutants had the same clonogenic radioresistance as cells with wild type (WT) receptors. Neither wortmannin nor LY294002, specific inhibitors of PI3-K, affected the radioresistance of cells with WT receptors at concentrations specific for PI3-K. Collectively, these results indicate that the PI3-K pathway is not essential for IGF-IR-mediated clonogenic radioresistance.
- 日本放射線影響学会の論文
著者
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Ryo Haruko
Dept. Of Radiation Biol. Faculty Of Med. Osaka Univ.
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Watanabe Hiromitsu
Research Institute for Radiation Biology and Medicine, Hiroshima University
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Watanabe Hiroshi
okyo Medical and Dental Univ.
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YU DONG
Molecular Diagnosis and Therapeutics
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MIURA MASAHIKO
Molecular Diagnosis and Therapeutics
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WATANABE HIROSHI
Oral and Maxillofacial Radiology, Graduate School, Tokyo Medical and Dental University
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SHIBUYA HITOSHI
Diagnostic Radiology and Oncology
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- The Phosphatidylinositol-3 kinase Pathway Is Not Essential for Insulin-like Growth Factor I Receptor-mediated Clonogenic Radioresistance.
- The Phosphatidylinositol-3 kinase Pathway Is Not Essential for Insulin-like Growth Factor I Receptor-mediated Clonogenic Radioresistance