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      The NF-κB Pathway and Cancer Stem Cells

      review-article
      Author(s): 1 , 2 , 2 , *
      Editor(s):
      Publication date (Electronic):
      Journal: Cells
      Publisher: MDPI
      Keywords: NF-κB, cancer, cancer stem cells, tumor-initiating cells, self-renewal

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          Abstract

          The NF-κB transcription factor pathway is a crucial regulator of inflammation and immune responses. Additionally, aberrant NF-κB signaling has been identified in many types of cancer. Downstream of key oncogenic pathways, such as RAS, BCR-ABL, and Her2, NF-κB regulates transcription of target genes that promote cell survival and proliferation, inhibit apoptosis, and mediate invasion and metastasis. The cancer stem cell model posits that a subset of tumor cells (cancer stem cells) drive tumor initiation, exhibit resistance to treatment, and promote recurrence and metastasis. This review examines the evidence for a role for NF-κB signaling in cancer stem cell biology.

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          Most cited references131

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          Identification of pancreatic cancer stem cells.

          Chenwei Li, David G Heidt, Piero Dalerba … (2007)
          Emerging evidence has suggested that the capability of a tumor to grow and propagate is dependent on a small subset of cells within a tumor, termed cancer stem cells. Although data have been provided to support this theory in human blood, brain, and breast cancers, the identity of pancreatic cancer stem cells has not been determined. Using a xenograft model in which primary human pancreatic adenocarcinomas were grown in immunocompromised mice, we identified a highly tumorigenic subpopulation of pancreatic cancer cells expressing the cell surface markers CD44, CD24, and epithelial-specific antigen (ESA). Pancreatic cancer cells with the CD44(+)CD24(+)ESA(+) phenotype (0.2-0.8% of pancreatic cancer cells) had a 100-fold increased tumorigenic potential compared with nontumorigenic cancer cells, with 50% of animals injected with as few as 100 CD44(+)CD24(+)ESA(+) cells forming tumors that were histologically indistinguishable from the human tumors from which they originated. The enhanced ability of CD44(+)CD24(+)ESA(+) pancreatic cancer cells to form tumors was confirmed in an orthotopic pancreatic tail injection model. The CD44(+)CD24(+)ESA(+) pancreatic cancer cells showed the stem cell properties of self-renewal, the ability to produce differentiated progeny, and increased expression of the developmental signaling molecule sonic hedgehog. Identification of pancreatic cancer stem cells and further elucidation of the signaling pathways that regulate their growth and survival may provide novel therapeutic approaches to treat pancreatic cancer, which is notoriously resistant to standard chemotherapy and radiation.
          Article 0 comments Cited 913 times – based on 0 reviews     Review now
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            Generation of neurons and astrocytes from isolated cells of the adult mammalian central nervous system.

            Kyle B. Reynolds, Thomas S. Weiss (1992)
            Neurogenesis in the mammalian central nervous system is believed to end in the period just after birth; in the mouse striatum no new neurons are produced after the first few days after birth. In this study, cells isolated from the striatum of the adult mouse brain were induced to proliferate in vitro by epidermal growth factor. The proliferating cells initially expressed nestin, an intermediate filament found in neuroepithelial stem cells, and subsequently developed the morphology and antigenic properties of neurons and astrocytes. Newly generated cells with neuronal morphology were immunoreactive for gamma-aminobutyric acid and substance P, two neurotransmitters of the adult striatum in vivo. Thus, cells of the adult mouse striatum have the capacity to divide and differentiate into neurons and astrocytes.
            Article 0 comments Cited 625 times – based on 0 reviews     Review now
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              NF-kappaB antiapoptosis: induction of TRAF1 and TRAF2 and c-IAP1 and c-IAP2 to suppress caspase-8 activation.

              C Y Wang, M. W. Mayo, R Korneluk … (1998)
              Tumor necrosis factor alpha (TNF-alpha) binding to the TNF receptor (TNFR) potentially initiates apoptosis and activates the transcription factor nuclear factor kappa B (NF-kappaB), which suppresses apoptosis by an unknown mechanism. The activation of NF-kappaB was found to block the activation of caspase-8. TRAF1 (TNFR-associated factor 1), TRAF2, and the inhibitor-of-apoptosis (IAP) proteins c-IAP1 and c-IAP2 were identified as gene targets of NF-kappaB transcriptional activity. In cells in which NF-kappaB was inactive, all of these proteins were required to fully suppress TNF-induced apoptosis, whereas c-IAP1 and c-IAP2 were sufficient to suppress etoposide-induced apoptosis. Thus, NF-kappaB activates a group of gene products that function cooperatively at the earliest checkpoint to suppress TNF-alpha-mediated apoptosis and that function more distally to suppress genotoxic agent-mediated apoptosis.
              Article 0 comments Cited 286 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Ruaidhri Carmody: Role: Academic Editor
                Journal
                Journal ID (nlm-ta): Cells
                Journal ID (iso-abbrev): Cells
                Journal ID (publisher-id): cells
                Title: Cells
                Publisher: MDPI
                ISSN (Electronic): 2073-4409
                Publication date (Electronic): 06 April 2016
                Publication date Collection: June 2016
                Volume: 5
                Issue: 2
                Electronic Location Identifier: 16
                Affiliations
                [1 ]Department of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, NC 27599, USA; arink@ 123456email.unc.edu
                [2 ]Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC 27599, USA
                Author notes
                [* ]Correspondence: albert_baldwin@ 123456med.unc.edu ; Tel.: +1-919-966-3652
                Article
                Publisher ID: cells-05-00016
                DOI: 10.3390/cells5020016
                PMC ID: 4931665
                PubMed ID: 27058560
                SO-VID: c694c73d-e490-416d-8993-a2ef319633bb
                Copyright © © 2016 by the authors; licensee MDPI, Basel, Switzerland.
                License:

                This article is an open access article distributed under the terms and conditions of the Creative Commons by Attribution (CC-BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 10 February 2016
                Date accepted : 31 March 2016
                Categories
                Subject: Review

                Keywords: nf-κb,cancer,cancer stem cells,tumor-initiating cells,self-renewal
                Data availability:
                Keywords: nf-κb, cancer, cancer stem cells, tumor-initiating cells, self-renewal

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