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請使用永久網址來引用或連結此文件:
http://ir.cmu.edu.tw/ir/handle/310903500/30426
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| 題名: | Clinical significance of serum soluble interleukin 2 receptor-alpha in esophageal squamous cell carcinoma |
| 作者: | Wang, LS;Chow, KC;Li, WY;Liu, CC;Wu, YC;Huang, MH |
| 貢獻者: | 附設醫院醫研部;Vet Gen Hosp, Dept Surg, Div Chest Surg, Taipei 11217, Taiwan;Vet Gen Hosp, Dept Pathol, Taipei, Taiwan;Natl Yang Ming Univ, Taipei 112, Taiwan;China Med Coll Hosp, Dept Med Res, Taipei 11217, Taiwan |
| 日期: | 2000 |
| 上傳時間: | 2010-09-24 14:55:11 (UTC+8) |
| 出版者: | AMER ASSOC CANCER RESEARCH |
| 摘要: | Purpose: Cyclooxygenase-2 (COX-2) is involved in antiapoptosis signaling, and its induction may require activation of protein kinase C (PKC). Safingol (SAF), a PKC inhibitor, has been shown to enhance apoptosis induced by mitomycin-C (MMC) in human gastric cancer MKN-74 cells. The aim of this study was to identify the role of COX-2 in MMC-induced apoptosis in MKN-74 cells. Methods: Protein expression of COX-2 and Bcl-2 and activation of PKC alpha were examined by Western blot analysis. Apoptosis induction was examined by staining with bisbenzimide trihydrochloride (Hoechst-33258) of condensed chromatin, which characterizes the cells undergoing apoptosis. COX-2 mRNA levels were examined by Northern blot analysis. Results: After exposure for 1-2 h to 1 mu g/ml MMC, upregulation of COX-2 and Bcl-2 protein expression was noted. The activation of PKC alpha occurred within 1 h of MMC exposure, and temporally preceded the induction of COX-2. Similar results were observed in cells exposed to the PKC activator, 3-phorbol 12-myristate 13-acetate. Cotreatment with SAF and MMC abolished the induction of COX-2 by MMC. Furthermore, NS-398, a selective COX-2 inhibitor, significantly enhanced MMC-induced apoptosis by fivefold from 4 +/- 2% (MMC alone) to 20 +/- 2% (MMC plus NS-398). There was no discernible change in COX-2 mRNA levels after a 2-h exposure to MMC but a twofold increase after a 24-h exposure. Conclusions: MMC upregulates COX-2 expression, which appears to be an antiapoptotic signal downstream of PKC. Selective inhibition of COX-2 can therefore provide a novel way to enhance MMC-induced apoptosis independent of inhibiting PKC. |
| 關聯: | CLINICAL CANCER RESEARCH 6(4):1445-1451 |
| 顯示於類別: | [台中附設醫院] 期刊論文
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