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      STAT3, stem cells, cancer stem cells and p63

      review-article
      Author(s): , ,
      Publication date (Electronic):
      Journal: Cellular & Molecular Biology Letters
      Publisher: BioMed Central
      Keywords: STAT3, Stem cells, Cancer stem cells, p63

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          Abstract

          Signal Transducer and Activator of Transcription 3 (STAT3) is a transcription factor with many important functions in the biology of normal and transformed cells. Its regulation is highly complex as it is involved in signaling pathways in many different cell types and under a wide variety of conditions. Besides other functions, STAT3 is an important regulator of normal stem cells and cancer stem cells. p63 which is a member of the p53 protein family is also involved in these functions and is both physically and functionally connected with STAT3. This review summarizes STAT3 function and regulation, its role in stem cell and cancer stem cell properties and highlights recent reports about its relationship to p63.

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          Most cited references138

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          p63 is essential for regenerative proliferation in limb, craniofacial and epithelial development.

          A. Yang, R Schweitzer, D. Sun … (1999)
          The p63 gene, a homologue of the tumour-suppressor p53, is highly expressed in the basal or progenitor layers of many epithelial tissues. Here we report that mice homozygous for a disrupted p63 gene have major defects in their limb, craniofacial and epithelial development. p63 is expressed in the ectodermal surfaces of the limb buds, branchial arches and epidermal appendages, which are all sites of reciprocal signalling that direct morphogenetic patterning of the underlying mesoderm. The limb truncations are due to a failure to maintain the apical ectodermal ridge, a stratified epithelium, essential for limb development. The embryonic epidermis of p63-/- mice undergoes an unusual process of non-regenerative differentiation, culminating in a striking absence of all squamous epithelia and their derivatives, including mammary, lacrymal and salivary glands. Taken together, our results indicate that p63 is critical for maintaining the progenitor-cell populations that are necessary to sustain epithelial development and morphogenesis.
          Article 0 comments Cited 465 times – based on 0 reviews     Review now
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            Jak-STAT pathways and transcriptional activation in response to IFNs and other extracellular signaling proteins.

            Shona Kerr, I Kerr, G Stark … (1994)
            Through the study of transcriptional activation in response to interferon alpha (IFN-alpha) and interferon gamma (IFN-gamma), a previously unrecognized direct signal transduction pathway to the nucleus has been uncovered: IFN-receptor interaction at the cell surface leads to the activation of kinases of the Jak family that then phosphorylate substrate proteins called STATs (signal transducers and activators of transcription). The phosphorylated STAT proteins move to the nucleus, bind specific DNA elements, and direct transcription. Recognition of the molecules involved in the IFN-alpha and IFN-gamma pathway has led to discoveries that a number of STAT family members exist and that other polypeptide ligands also use the Jak-STAT molecules in signal transduction.
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              p63, a p53 homolog at 3q27-29, encodes multiple products with transactivating, death-inducing, and dominant-negative activities.

              A. Yang, M Kaghad, Y Wang … (1998)
              We describe the cloning of p63, a gene at chromosome 3q27-29 that bears strong homology to the tumor suppressor p53 and to the related gene, p73. p63 was detected in a variety of human and mouse tissues, including proliferating basal cells of epithelial layers in the epidermis, cervix, urothelium, and prostate. Unlike p53, the p63 gene encodes multiple isotypes with remarkably divergent abilities to transactivate p53 reporter genes and induce apoptosis. Importantly, the predominant p63 isotypes in many epithelial tissues lack an acidic N terminus corresponding to the transactivation domain of p53. We demonstrate that these truncated p63 variants can act as dominant-negative agents toward transactivation by p53 and p63, and we suggest the possibility of physiological interactions among members of the p53 family.
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                Author and article information

                Contributors
                Michaela Galoczova:
                ORCID: http://orcid.org/0000-0002-2016-821X
                michaela.galoczova@mou.cz
                Philip Coates: philip.coates@mou.cz
                Borivoj Vojtesek: vojtesek@mou.cz
                Journal
                Journal ID (nlm-ta): Cell Mol Biol Lett
                Journal ID (iso-abbrev): Cell. Mol. Biol. Lett
                Title: Cellular & Molecular Biology Letters
                Publisher: BioMed Central (London )
                ISSN (Print): 1425-8153
                ISSN (Electronic): 1689-1392
                Publication date (Electronic): 22 March 2018
                Publication date PMC-release: 22 March 2018
                Publication date Collection: 2018
                Volume: 23
                Electronic Location Identifier: 12
                Affiliations
                GRID grid.419466.8, Regional Centre for Applied Molecular Oncology, , Masaryk Memorial Cancer Institute, ; Zluty kopec 7, 656 53 Brno, Czech Republic
                Author information
                http://orcid.org/0000-0002-2016-821X
                Article
                Publisher ID: 78
                DOI: 10.1186/s11658-018-0078-0
                PMC ID: 5863838
                PubMed ID: 29588647
                SO-VID: 0b36ff61-c6ee-4464-934a-4b871043a0eb
                Copyright © © The Author(s) 2018
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Date received : 15 December 2017
                Date accepted : 7 March 2018
                Funding
                Funded by: MEYS - NPS 1
                Award ID: LO1413
                Funded by: FundRef http://dx.doi.org/10.13039/501100001824, Grantová Agentura České Republiky;
                Award ID: P206/12/G151
                Award Recipient :
                Funded by: MH CZ - DRO
                Award ID: MMCI, 00209805
                Categories
                Subject: Review
                Custom metadata
                issue-copyright-statement © The Author(s) 2018

                Keywords: stat3,stem cells,cancer stem cells,p63
                Data availability:
                Keywords: stat3, stem cells, cancer stem cells, p63

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