Tumor promoting or tumor suppressing of NF-κB, a matter of cell context dependency

被引:30
作者
Chen, Fei [1 ]
Beezhold, Kevin [1 ]
Castranova, Vince [2 ]
机构
[1] NIOSH, Pathol & Physiol Res Branch, Hlth Effects Lab Div, Morgantown, WV USA
[2] W Virginia Univ, Dept Physiol & Pharmacol, Sch Med, Morgantown, WV 26506 USA
关键词
NF-kappa B; JNK; ROS; tumor suppressing; epigenetics; histone methylation;
D O I
10.1080/08830180802130327
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Nuclear factor-kappa B (NF-kappa B) and its activating signaling pathways are critical regulators for cell lineage development, growth, differentiation, apoptosis, and tumorigenic transformation. As one of the most important transcription factors, NF-kappa B has been implicated in the transcriptional upregulation of a number of cytokines, adhesion molecules, growth factors, oncogenes, antiapoptotic proteins, some proapoptotic factors, and even certain viral genes. The role of NF-kappa B on tumor promoting has been well-documented in the past two decades. However, during the past few years, a considerable number of studies suggested that NF-kappa B and its activating signaling molecules may act as tumor suppressors under some circumstances. Thus, it is highly possible that tumor promoting or tumor suppressing of NF-kappa B signaling is determined by the type of cells, stimuli, simultaneous or asynchronous intracellular signals, and other cellular contexts.
引用
收藏
页码:183 / 204
页数:22
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