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      Is Open Access

      To NFκB or not to NFκB: The Dilemma on How to Inhibit a Cancer Cell Fate Regulator

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          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Nuclear factor κB (NFκB) is a transcription factor that plays an important role in carcinogenesis as well as in the regulation of inflammatory response. NFκB is constitutively expressed in tumours where it induces the expression of genes which promote cell proliferation, apoptotic events, angiogenesis, invasion and metastasis. Furthermore, many cancer cells show aberrant or constitutive NFκB activation that mediates resistance to chemo- and radio-therapy. Therefore, the inhibition of NFκB activity appears a potential therapeutic strategy for cancer treatment. In this review, we focus on the role of NFκB in carcinogenesis and summarize actual inhibitors of NFκB that could be potential therapeutic target in cancer therapy.

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          Most cited references126

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          Mdm2 promotes the rapid degradation of p53.

          Y Haupt, R Maya, A Kazaz … (1997)
          The p53 tumour-suppressor protein exerts antiproliferative effects, including growth arrest and apoptosis, in response to various types of stress. The activity of p53 is abrogated by mutations that occur frequently in tumours, as well as by several viral and cellular proteins. The Mdm2 oncoprotein is a potent inhibitor of p53. Mdm2 binds the transcriptional activation domain of p53 and blocks its ability to regulate target genes and to exert antiproliferative effects. On the other hand, p53 activates the expression of the mdm2 gene in an autoregulatory feedback loop. The interval between p53 activation and consequent Mdm2 accumulation defines a time window during which p53 exerts its effects. We now report that Mdm2 also promotes the rapid degradation of p53 under conditions in which p53 is otherwise stabilized. This effect of Mdm2 requires binding of p53; moreover, a small domain of p53, encompassing the Mdm2-binding site, confers Mdm2-dependent detstabilization upon heterologous proteins. Raised amounts of Mdm2 strongly repress mutant p53 accumulation in tumour-derived cells. During recovery from DNA damage, maximal Mdm2 induction coincides with rapid p53 loss. We propose that the Mdm2-promoted degradation of p53 provides a new mechanism to ensure effective termination of the p53 signal.
          Article 0 comments Cited 836 times – based on 0 reviews     Review now
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            Extrinsic versus intrinsic apoptosis pathways in anticancer chemotherapy.

            S Fulda, K-M Debatin (2006)
            Apoptosis or programmed cell death is a key regulator of physiological growth control and regulation of tissue homeostasis. One of the most important advances in cancer research in recent years is the recognition that cell death mostly by apoptosis is crucially involved in the regulation of tumor formation and also critically determines treatment response. Killing of tumor cells by most anticancer strategies currently used in clinical oncology, for example, chemotherapy, gamma-irradiation, suicide gene therapy or immunotherapy, has been linked to activation of apoptosis signal transduction pathways in cancer cells such as the intrinsic and/or extrinsic pathway. Thus, failure to undergo apoptosis may result in treatment resistance. Understanding the molecular events that regulate apoptosis in response to anticancer chemotherapy, and how cancer cells evade apoptotic death, provides novel opportunities for a more rational approach to develop molecular-targeted therapies for combating cancer.
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              NF-kappaB in cancer: from innocent bystander to major culprit.

              Michael Karin, Yixue Cao, Florian Greten … (2002)
              Nuclear factor of kappaB (NF-kappaB) is a sequence-specific transcription factor that is known to be involved in the inflammatory and innate immune responses. Although the importance of NF-KB in immunity is undisputed, recent evidence indicates that NF-kappaB and the signalling pathways that are involved in its activation are also important for tumour development. NF-kappaB should therefore receive as much attention from cancer researchers as it has already from immunologists.
              Article 0 comments Cited 541 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Transl Med UniSa
                Journal ID (iso-abbrev): Transl Med UniSa
                Title: Translational Medicine @ UniSa
                Publisher: Università di Salerno
                ISSN (Print): 2239-9747
                ISSN (Electronic): 2239-9747
                Publication date (Electronic): 11 October 2012
                Publication date Collection: Sep-Dec 2012
                Volume: 4
                Pages: 73-85
                Affiliations
                [1 ]Department of Clinical Medicine, Cardiovascular and Immunological Science, Federico II University of Naples, Italy
                [2 ]Department of Cellular and Molecular Biology and Pathology, Federico II University of Naples, Italy
                [3 ]Department of Medicine and Surgery, University of Salerno, Italy
                [4 ]IRCCS “Multimedica”, Milano, Italy
                Author notes
                Address Correspondence to Guido Iaccarino MD, PhD, FESC, ( giaccarino@ 123456unisa.it )
                Article
                Publisher ID: tm-04-73
                PMC ID: 3728801
                PubMed ID: 23905066
                SO-VID: fcffb7b5-48fb-4e7f-99a3-daa753ddc6c5
                Copyright statement: Copyright @ 2012
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Categories
                Subject: Review

                Keywords: transcription factors,iκb,grk5,cancer
                Data availability:
                Keywords: transcription factors, iκb, grk5, cancer

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