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: NPXY⁹⁵⁰ and Y¹³¹⁶XXM. 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.<br>

• Journal of Radiation Research 編集委員会の論文

著者

• WATANABE Hiroshi

  Oral Maxillofac. Radiol. Tokyo Med. and Dent. Univ.

• Shibuya Hitoshi

  Diagnostic Radiology And Oncology Graduate School Tokyo Medical And Dental University

• YU DONG

  Molecular Diagnosis and Therapeutics

• MIURA MASAHIKO

  Molecular Diagnosis and Therapeutics

• WATANABE HIROSHI

  Oral and Maxillofacial Radiology, Graduate School, Tokyo Medical and Dental University

• 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

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