Thromboxane synthase suppression induces lung cancer cell apoptosis via inhibiting NF-kappa B
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摘要Accumulating evidence shows that the inhibition of thromboxane synthase (TXS) induced apoptosis in cancer cells. TXS inhibitor 1-Benzylimidzole (1-BI) can trigger apoptosis in lung cancer cells but the mechanism is not fully defined. In this study, lung cancer cells were treated with 1-BI. In this study, the level of reactive oxygen species (ROS) was measured and NF-kappa B activity was determined in human lung cancer cells. The roles of ROS and NF-kappa B in 1-BI-mediated cell death were analyzed. The results showed that 1-BI induced ROS generation but decreased the activity of NF-kappa B by reducing phosphorylated I kappa B alpha (p-1 kappa B alpha) and inhibiting the translocation of p65 into the nucleus. In contrast to 1-BI, antioxidant N-acetyl cysteine (NAC) stimulated cell proliferation and significantly protected the cells from 1-BI-mediated cell death by neutralizing ROS. Collectively, apoptosis induced by 1-BI is associated with the over-production of ROS and the reduction of NF-kappa B. Antioxidants can significantly block the inhibitory effect of 1-BI. (C) 2010 Elsevier Inc. All rights reserved.
著者Leung KC, Li MY, Leung BCS, Hsin MKY, Mok TSK, Underwood MJ, Chen GG
期刊名稱Experimental Cell Research
出版年份2010
月份12
日期10
卷號316
期次20
出版社ELSEVIER INC
頁次3468 - 3477
國際標準期刊號0014-4827
電子國際標準期刊號1090-2422
語言英式英語
關鍵詞Apoptosis; Lung cancer; Nuclear factor kappaB; Oxidative stress; Thromboxane synthase
Web of Science 學科類別Cell Biology; CELL BIOLOGY; Oncology; ONCOLOGY

上次更新時間 2020-26-11 於 01:03