| First Author | Legge DN | Year | 2020 |
| Journal | Carcinogenesis | Volume | 41 |
| Issue | 3 | Pages | 249-256 |
| PubMed ID | 31930327 | Mgi Jnum | J:289108 |
| Mgi Id | MGI:6416743 | Doi | 10.1093/carcin/bgaa003 |
| Citation | Legge DN, et al. (2020) The role of B-Cell Lymphoma-3 (BCL-3) in enabling the hallmarks of cancer: implications for the treatment of colorectal carcinogenesis. Carcinogenesis 41(3):249-256 |
| abstractText | With its identification as a proto-oncogene in chronic lymphocytic leukaemia and central role in regulating NF-kappaB 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. |
