Thromboxane synthase suppression induces lung cancer cell apoptosis via inhibiting NF-kappa B
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AbstractAccumulating 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.
All Author(s) ListLeung KC, Li MY, Leung BCS, Hsin MKY, Mok TSK, Underwood MJ, Chen GG
Journal nameExperimental Cell Research
Volume Number316
Issue Number20
Pages3468 - 3477
LanguagesEnglish-United Kingdom
KeywordsApoptosis; Lung cancer; Nuclear factor kappaB; Oxidative stress; Thromboxane synthase
Web of Science Subject CategoriesCell Biology; CELL BIOLOGY; Oncology; ONCOLOGY

Last updated on 2021-20-09 at 00:04