Premium
Role of WWOX and NF‐κB in lung cancer progression (1049.2)
Author(s) -
Chang NanShan
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1049.2
Subject(s) - wwox , cancer research , transcription factor , nf κb , tumor necrosis factor alpha , suppressor , lung cancer , nfkb1 , signal transduction , phosphorylation , biology , cancer , medicine , microbiology and biotechnology , immunology , gene , genetics
The pro‐inflammatory, pro‐survival transcription factor NF‐κB is considered as 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. Grant Funding Source : NSC and NHRI, Taiwan, and DoD, USA