Journal
CARCINOGENESIS
Volume 41, Issue 3, Pages 249-256Publisher
OXFORD UNIV PRESS
DOI: 10.1093/carcin/bgaa003
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Funding
- Bowel & Cancer Research PhD studentship
- MRC clinical research training fellowship [MR/N001494/1]
- Wellcome Trust Four Year PhD Programme in Dynamic Molecular Cell Biology [203988/Z/16Z]
- MRC Research grant [MR/R017247/1]
- John James Bristol Foundation
- MRC [MR/N001494/1, MR/R017247/1] Funding Source: UKRI
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With its identification as a proto-oncogene in chronic lymphocytic leukaemia and central role in regulating NF-kappa B signalling, it is perhaps not surprising that there have been an increasing number of studies in recent years investigating the role of BCL-3 (B-Cell Chronic Lymphocytic Leukaemia/Lymphoma-3) in a wide range of human cancers. Importantly, this work has begun to shed light on our mechanistic understanding of the function of BCL-3 in tumour promotion and progression. Here, we summarize the current understanding of BCL-3 function in relation to the characteristics or traits associated with tumourigenesis, termed 'Hallmarks of Cancer'. With the focus on colorectal cancer, a major cause of cancer related mortality in the UK, we describe the evidence that potentially explains why increased BCL-3 expression is associated with poor prognosis in colorectal cancer. As well as promoting tumour cell proliferation, survival, invasion and metastasis, a key emerging function of this proto-oncogene is the regulation of the tumour response to inflammation. We suggest that BCL-3 represents an exciting new route for targeting the Hallmarks of Cancer; in particular by limiting the impact of the enabling hallmarks of tumour promoting inflammation and cell plasticity. As BCL-3 has been reported to promote the stem-like potential of cancer cells, we suggest that targeting BCL-3 could increase the tumour response to conventional treatment, reduce the chance of relapse and hence improve the prognosis for cancer patients.
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