Interruption of Hepatocyte Growth Factor Signaling Augmented Oridonin-Induced Death in Human Non-small Cell Lung Cancer A549 Cells via c-Met-Nuclear Factor-κB-Cyclooxygenase-2 and c-Met-Bcl-2-Caspase-3 Pathways
スポンサーリンク
概要
- 論文の詳細を見る
The aim of this study was to elucidate the molecular mechanisms mediating hepatocyte growth factor (HGF)-induced protection against oridonin-induced apoptosis in A549 cells. Oridonin induced decrease in Bcl-2/Bax ratio and activation of caspase-3, while these processes were reversed by HGF, suggesting that HGF played an anti-apoptotic role in oridonin-induced A549 cell death. HGF-induced protective effect was partially attributed to the activation of nuclear factor (NF)-κB and cyclooxygenase 2 (COX-2), since the protective effect was abolished by inhibition of NF-κB or interruption of COX-2. Then the activated COX-2 could prevent cells from initiating the apoptotic response by promoting prostaglandin E2 (PGE2) release. Activation of NF-κB-COX-2 by HGF-treatment triggered the increase in Bcl-2/Bax ratio, inhibition of procaspase-3 cleavage, promotion of Ca2+-independent intracellular phospholipase A2 (iPLA2) expression and augmentation of PGE2 release, leading to antagonizing oridonin-induced cell death in A549 cells. HGF-induced cell survival in response to oridonin administration was associated with the activation of c-Met-NF-κB-COX-2 and c-Met-Bcl-2-caspase-3 signaling pathways. iPLA2, downstream effector of caspase-3, also participated in these processes.
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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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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Shi Qi-feng
China-japan Research Institute Of Medical And Pharmaceutical Sciences Shenyang Pharmaceutical University
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Qi Min
China-Japan Research Institute of Medical and Pharmaceutical Sciences, Shenyang Pharmaceutical University
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IKEJIMA Takashi
China-Japan Research Institute of Medical and Pharmaceutical Sciences, Shenyang Pharmaceutical University
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Ikejima Takashi
China–Japan Research Institute of Medical and Pharmaceutical Sciences, Shenyang Pharmaceutical University
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