Thromboxane synthase suppression induces lung cancer cell apoptosis via inhibiting NF-κB

Experimental Cell Research
Kin Chung LeungGeorge G Chen

Abstract

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-κB activity was determined in human lung cancer cells. The roles of ROS and NF-κB in 1-BI-mediated cell death were analyzed. The results showed that 1-BI induced ROS generation but decreased the activity of NF-κB by reducing phosphorylated IκBα (p-IκBα) 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-κB. Antioxidants can significantly block the inhibitory effect of 1-BI.

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Citations

Jun 15, 2013·Oxidative Medicine and Cellular Longevity·Michelle R CampbellDouglas A Bell
Oct 18, 2011·Cancer Metastasis Reviews·Claus Schneider, Ambra Pozzi
Jun 5, 2015·Acta Biochimica Et Biophysica Sinica·Guang-Zhe GeCeshi Chen
Jan 21, 2015·Pharmacology & Therapeutics·Michael MurrayTristan Rawling
Feb 1, 2014·Biochimica Et Biophysica Acta·Mary Clare CathcartGraham P Pidgeon
Mar 19, 2016·Vascular Pharmacology·Josiane F SilvaVirginia S Lemos

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