Special Issue "NF-κB in Cancer"
A special issue of Cells (ISSN 2073-4409).
Deadline for manuscript submissions: closed (30 June 2018)
Prof. Dr. Neil D. Perkins
Institute for Cell and Molecular Biosciences (ICaMB), Medical School, Newcastle University, Catherine Cookson Building, Framlington Place, Newcastle upon Tyne, NE2 4HH, United Kingdom
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Phone: +44 (0) 191 208 8866
Fax: +44 (0) 191 208 7424
Interests: NF-κB; DNA damage; p53; CHK1; cancer; phosphorylation; cell signalling
It is now well established that aberrant activation of the NF-κB signalling pathway can drive cancer development and malignancy in both tumour and non-tumour cell types. Consequently, it represents an attractive drug target for the treatment of a broad range of cancer.
Under normal circumstances, NF-κB is an important regulator of the immune and inflammatory responses and comprises a family of dimeric transcription factors with common and distinct biological functions. NF-κB complexes, formed from a family of five NF-κB subunits, RelA (p65), c-Rel, RelB, NF-κB1 (p105/p50) and NF-κB2 (p100/p52), are present in all cells, but are generally held in an inactive form until induced by wide range of stimuli, including inflammatory cytokines, cell stresses such as DNA damage or hypoxia, immune receptor engagement, bacterial products and viral proteins. There are, broadly speaking, two major pathways leading to induction of NF-κB subunits. The classical (or canonical) pathway typically leads to the induction of RelA(p65) or c-Rel containing complexes and involves the degradation of IκBα in a manner dependent on IκB kinase (IKK) beta and the IKK regulatory subunit NEMO (IKKγ). The non-canonical (or alternative) pathway, involves the inducible processing of p100 to p52, leading to the induction of p52/RelB containing complexes, and is dependent on IKKα and NF-κB inducing kinase (NIK).
Aberrantly active NF-κB, induced by both the classical and non-canonical pathways, contributes to the pathology of many diseases, including cancer. In cancer, NF-κB activation only rarely results from direct mutation of the NF-κB or IKK subunits but most commonly arises either through mutation of upstream regulators leading to constitutive IKK activity or via effects of the tumour microenvironment. Its critical role in the inflammatory phenotype allows NF-κB to act as a promoter of inflammation-associated cancers. However, activation of NF-κB in tumour cells can induce many genes that regulate many of the 'Hallmarks of Cancer' and so can promote cancer progression, increased metastatic potential, tumour recurrence and therapeutic resistance in a wide range of both solid and haematological malignancies. Consequently, there is often an assumption that NF-κB is an obligate tumour promoter. However, tumour suppressor-like characteristics associated with NF-κB subunits have also been described. Understanding the complexity of NF-κB cancer biology will be required if we are to fully exploit its potential as a therapeutic target.
The aim of this special issue is to provide an overview of the broad role that NF-κB plays in cancer. This will include both its function as a driver of inflammation associated cancer and its function as an effector of oncogene induced malignancy. However, we will also cover the links between NF-κB and tumour suppressors and how these can lead to altered NF-κB behaviour in some contexts. We will cover the mechanisms leading to aberrant NF-κB in cancer, the functions of the NF-κB subunits themselves and consider, given the complexity of the pathway, the best strategies for targeting it to achieve new and improved cancer therapies.
Prof. Dr. Neil D. Perkins
Manuscript Submission Information
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- Tumour Suppressors
- Cancer Therapy