The endogenous reactive oxygen species promote NF-kappaB activation by targeting on activation of NF-kappaB-inducing kinase in oral squamous carcinoma cells |
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Authors: | Wang Yumei Huang Xinzhi Cang Hui Gao Fei Yamamoto Tetsuya Osaki Tokio Yi Jing |
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Institution: |
a Department of Cell Biology, Key Laboratory of the Education Ministry of China for Cell Differentiation and Apoptosis, Shanghai Jiao Tong University School of Medicine, Shanghai, China
b Department of Oral and Maxillofacial Surgery, Kochi medical School, Kochi University, Nankoku, Japan |
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Abstract: | Reactive oxygen species (ROS) could stimulate or inhibit NF-κB pathways. However, most results have been obtained on the basis of the exogenous ROS and the molecular target of ROS in NF-κB signalling pathways has remained unclear. Here, the oral squamous carcinoma (OSC) cells, with a mild difference in the endogenous ROS level, were used to investigate how slight fluctuation of the endogenous ROS regulates NF-κB activation. This study demonstrates that NF-κB-inducing kinase (NIK) is a critical target of the endogenous ROS in NF-κB pathways. The results indicate that ROS may function as a physiological signalling modulator on NF-κB signalling cascades through its ability to facilitate the activity of NIK and subsequent NF-κB transactivation. In addition, the data are useful to explain why the altered intracellular microenvironment related to redox state may influence biological behaviours of cancer cells. |
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Keywords: | Endogenous ROS NIK NF-κB |
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