Title |
Role of WWOX and NF-κB in lung cancer progression
|
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Published in |
Translational Respiratory Medicine, November 2013
|
DOI | 10.1186/2213-0802-1-15 |
Pubmed ID | |
Authors |
Szu-Jung Chen, Shenq-Shyang Huang, Nan-Shan Chang |
Abstract |
It is generally agreed that the pro-inflammatory, pro-survival transcription factor NF-κB is a tumor promoter. Tumor necrosis factor alpha (TNF-α or TNF) mediates NF-κB activation. Tumor suppressor WWOX (FOR or WOX1) is a downstream effector of the TNF signaling. Thus, activation of both WWOX (FOR or WOX1) and NF-κB may occur during TNF signaling and/or under stress conditions. Indeed, the first WW domain of WWOX induces the activation of NF-κB-responsive promoter without TNF participation. It appears that WWOX counteracts with NF-κB in regulating cell survival and death. For example, WWOX becomes activated with Tyr33 phosphorylation and relocates together with NF-κB and many transcription factors to the nucleus to cause neuronal death in sciatic nerve-transected rats. While WWOX is frequently lost in lung cancer and many other cancers, NF-κB activation-induced cancer promotion probably requires WWOX-independent signaling networks to induce expression of pro-survival factors. The antagonistic role of WWOX and NF-κB in the regulation of lung cancer progression is discussed. |
Mendeley readers
Geographical breakdown
Country | Count | As % |
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Unknown | 13 | 100% |
Demographic breakdown
Readers by professional status | Count | As % |
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Researcher | 4 | 31% |
Student > Master | 3 | 23% |
Other | 2 | 15% |
Student > Bachelor | 2 | 15% |
Student > Ph. D. Student | 1 | 8% |
Other | 1 | 8% |
Readers by discipline | Count | As % |
---|---|---|
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Medicine and Dentistry | 5 | 38% |
Biochemistry, Genetics and Molecular Biology | 1 | 8% |
Chemistry | 1 | 8% |
Pharmacology, Toxicology and Pharmaceutical Science | 1 | 8% |
Other | 0 | 0% |