NFKB1 and Cancer: Friend or Foe?

被引:98
作者
Concetti, Julia [1 ]
Wilson, Caroline L. [1 ]
机构
[1] Newcastle Univ, Inst Cellular Med, Newcastle Fibrosis Res Grp, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England
关键词
NF-kappa B; NFKB1; p105/p50; Bcl-3; cancer; inflammation; apoptosis; NF-KAPPA-B; INSERTION/DELETION ATTG POLYMORPHISM; LEUKEMIA; 3; BCL-3; CONSTITUTIVE ACTIVATION; TRANSCRIPTION FACTORS; PROMOTER REGION; GENE INCREASES; POOR-PROGNOSIS; INFLAMMATORY RESPONSES; COLORECTAL-CANCER;
D O I
10.3390/cells7090133
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Current evidence strongly suggests that aberrant activation of the NF-kappa B signalling pathway is associated with carcinogenesis. A number of key cellular processes are governed by the effectors of this pathway, including immune responses and apoptosis, both crucial in the development of cancer. Therefore, it is not surprising that dysregulated and chronic NF-kappa B signalling can have a profound impact on cellular homeostasis. Here we discuss NFKB1 (p105/p50), one of the five subunits of NF-kappa B, widely implicated in carcinogenesis, in some cases driving cancer progression and in others acting as a tumour-suppressor. The complexity of the role of this subunit lies in the multiple dimeric combination possibilities as well as the different interacting co-factors, which dictate whether gene transcription is activated or repressed, in a cell and organ-specific manner. This review highlights the multiple roles of NFKB1 in the development and progression of different cancers, and the considerations to make when attempting to manipulate NF-kappa B as a potential cancer therapy.
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页数:16
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