Hypoxia and Inflammation in Cancer, Focus on HIF and NF-κB

被引:155
作者
D'Ignazio, Laura [1 ]
Batie, Michael [1 ]
Rocha, Sonia [1 ]
机构
[1] Univ Dundee, Sch Life Sci, Ctr Gene Regulat & Express, Dundee DD15EH, Scotland
基金
英国惠康基金; 英国医学研究理事会;
关键词
NF-kappa B; hypoxia; inflammation; kappa B Kinase (IKK); Prolyl Hydroxylases (PHDs); cancer; Transforming Growth Factor-beta-Activated Kinase 1 (TAK1); Factor Inhibiting HIF (FIH); ENDOTHELIAL GROWTH-FACTOR; RENAL-CELL CARCINOMA; EPITHELIAL-MESENCHYMAL TRANSITION; DEPENDENT GENE-EXPRESSION; INDUCIBLE FACTOR 2-ALPHA; LYMPH-NODE METASTASIS; BREAST-CANCER; COLORECTAL-CANCER; C-MYC; HISTONE DEMETHYLASES;
D O I
10.3390/biomedicines5020021
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Cancer is often characterised by the presence of hypoxia and inflammation. Paramount to the mechanisms controlling cellular responses under such stress stimuli, are the transcription factor families of Hypoxia Inducible Factor (HIF) and Nuclear Factor of -light-chain-enhancer of activated B cells (NF-kappa B). Although, a detailed understating of how these transcription factors respond to their cognate stimulus is well established, it is now appreciated that HIF and NF-kappa B undergo extensive crosstalk, in particular in pathological situations such as cancer. Here, we focus on the current knowledge on how HIF is activated by inflammation and how NF-kappa B is modulated by hypoxia. We summarise the evidence for the possible mechanism behind this activation and how HIF and NF-kappa B function impacts cancer, focusing on colorectal, breast and lung cancer. We discuss possible new points of therapeutic intervention aiming to harness the current understanding of the HIF-NF-kappa B crosstalk.
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页数:23
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