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

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.

journal_name

Exp Cell Res

authors

Leung KC,Li MY,Leung BC,Hsin MK,Mok TS,Underwood MJ,Chen GG

doi

10.1016/j.yexcr.2010.07.003

subject

Has Abstract

pub_date

2010-12-10 00:00:00

pages

3468-77

issue

20

eissn

0014-4827

issn

1090-2422

pii

S0014-4827(10)00365-4

journal_volume

316

pub_type

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