Activated O<SUB>2</SUB><SUP>•−</SUP> and H<SUB>2</SUB>O<SUB>2</SUB> Mediated Cell Survival in SU11274-Treated Non-Small-Cell Lung Cancer A549 Cells via c-Met–PI3K–Akt and c-Met–Grb2/SOS–Ras–p38 Pathways
スポンサーリンク
概要
- 論文の詳細を見る
The pharmacological activity of SU11274 is primarily due to its inhibition of hepotocyte growth factor receptor (c-Met) kinase overexpression. In this study, we demonstrated that the pathway involved in SU11274-induced autophagy was presumably through inhibition of c-Met and its down-stream pathways, including phosphatidylinositol 3-kinases – Akt (PI3K–Akt) and the growth factor receptor bound protein-2 / son of sevenless – Ras – p38 MAPK (Grb2/SOS–Ras–p38) pathway. SU11274 time-dependently induced the generation of superoxide anion (O<SUB>2</SUB><SUP>•−</SUP>) and hydrogen peroxide (H<SUB>2</SUB>O<SUB>2</SUB>). There is a negative feedback loop between reactive oxygen species (ROS) induction and SU11274. Then, we investigated the role of ROS in protecting cells against SU11274-induced autophagic cell death in A549 cells. O<SUB>2</SUB><SUP>•−</SUP> and H<SUB>2</SUB>O<SUB>2</SUB> generation activated c-Met–PI3K–Akt and c-Met–Grb2/SOS–Ras–p38 signaling pathways, which were suppressed by O<SUB>2</SUB><SUP>•−</SUP> scavenger superoxide dismutase (SOD) and H<SUB>2</SUB>O<SUB>2</SUB> scavenger catalase. In conclusion, O<SUB>2</SUB><SUP>•−</SUP> and H<SUB>2</SUB>O<SUB>2</SUB> evoked cell resistance to SU11274 via activating c-Met–PI3K–Akt and c-Met–Grb2/SOS–Ras–p38 pathways in A549 cells. SU11274 also induced ROS generation in <I>Caenorhabditis elegans</I>.
著者
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Ikejima Takashi
China-japan Res. Inst. Of Medical And Pharmaceutical Sciences Shenyang Pharmaceutical Univ. Chn
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Onodera Satoshi
Department Of Cinical And Biomedical Sciences Showa Pharmaceutical University
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Tashiro Shin-ichi
Department Of Cinical And Biomedical Sciences Showa Pharmaceutical University
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Ye Yuan-chao
China-japan Research Institute Of Medical And Pharmaceutical Sciences Shenyang Pharmaceutical University
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LIU Ying
China-Japan Research Institute of Medical and Pharmaceutical Sciences, Shenyang Pharmaceutical University
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Shi Qi-feng
China-japan Research Institute Of Medical And Pharmaceutical Sciences Shenyang Pharmaceutical University
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