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      Regulation of C-X-C chemokine gene expression by keratin 17 and hnRNP K in skin tumor keratinocytes

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          Abstract

          Interaction between K17 and hnRNP K regulates CXCR3 signaling in an RSK-dependent fashion to promote epithelial tumor cell growth and invasion.

          Abstract

          High levels of the intermediate filament keratin 17 (K17) correlate with a poor prognosis for several types of epithelial tumors. However, the causal relationship and underlying mechanisms remain undefined. A recent study suggested that K17 promotes skin tumorigenesis by fostering a specific type of inflammation. We report here that K17 interacts with the RNA-binding protein hnRNP K, which has also been implicated in cancer. K17 is required for the cytoplasmic localization of hnRNP K and for its role in regulating the expression of multiple pro-inflammatory mRNAs. Among these are the CXCR3 ligands CXCL9, CXCL10, and CXCL11, which together form a signaling axis with an established role in tumorigenesis. The K17–hnRNP K partnership is regulated by the ser/thr kinase RSK and required for CXCR3-dependent tumor cell growth and invasion. These findings functionally integrate K17, hnRNP K, and gene expression along with RSK and CXCR3 signaling in a keratinocyte-autonomous axis and provide a potential basis for their implication in tumorigenesis.

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          Most cited references38

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          The RSK family of kinases: emerging roles in cellular signalling.

          Rana Anjum, John Blenis (2008)
          The 90 kDa ribosomal S6 kinase (RSK) family of proteins is a group of highly conserved Ser/Thr kinases that regulate diverse cellular processes, such as cell growth, cell motility, cell survival and cell proliferation. RSKs are downstream effectors of the Ras-extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) signalling cascade. Significant advances in the field of RSK and ERK/MAPK signalling have occurred in the past few years, including biological insights and the discovery of novel substrates and new RSK regulatory mechanisms. Collectively, these data expand the current models of RSK signalling and highlight potential directions of research in RSK-mediated survival, growth, proliferation and migration.
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            A keratin cytoskeletal protein regulates protein synthesis and epithelial cell growth.

            P Coulombe, Pauline Wong, Seyun Kim (2006)
            Cell growth, an increase in mass and size, is a highly regulated cellular event. The Akt/mTOR (mammalian target of rapamycin) signalling pathway has a central role in the control of protein synthesis and thus the growth of cells, tissues and organisms. A striking example of a physiological context requiring rapid cell growth is tissue repair in response to injury. Here we show that keratin 17, an intermediate filament protein rapidly induced in wounded stratified epithelia, regulates cell growth through binding to the adaptor protein 14-3-3sigma. Mouse skin keratinocytes lacking keratin 17 (ref. 4) show depressed protein translation and are of smaller size, correlating with decreased Akt/mTOR signalling activity. Other signalling kinases have normal activity, pointing to the specificity of this defect. Two amino acid residues located in the amino-terminal head domain of keratin 17 are required for the serum-dependent relocalization of 14-3-3sigma from the nucleus to the cytoplasm, and for the concomitant stimulation of mTOR activity and cell growth. These findings reveal a new and unexpected role for the intermediate filament cytoskeleton in influencing cell growth and size by regulating protein synthesis.
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              Ribosomal protein S3: a KH domain subunit in NF-kappaB complexes that mediates selective gene regulation.

              Vijay Hegde, Lloyd Lam, K. Anderson … (2007)
              NF-kappaB is a DNA-binding protein complex that transduces a variety of activating signals from the cytoplasm to specific sets of target genes. To understand the preferential recruitment of NF-kappaB to specific gene regulatory sites, we used NF-kappaB p65 in a tandem affinity purification and mass spectrometry proteomic screen. We identified ribosomal protein S3 (RPS3), a KH domain protein, as a non-Rel subunit of p65 homodimer and p65-p50 heterodimer DNA-binding complexes that synergistically enhances DNA binding. RPS3 knockdown impaired NF-kappaB-mediated transcription of selected p65 target genes but not nuclear shuttling or global protein translation. Rather, lymphocyte-activating stimuli caused nuclear translocation of RPS3, parallel to p65, to form part of NF-kappaB bound to specific regulatory sites in chromatin. Thus, RPS3 is an essential but previously unknown subunit of NF-kappaB involved in the regulation of key genes in rapid cellular activation responses. Our observations provide insight into how NF-kappaB selectively controls gene expression.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Cell Biol
                Journal ID (iso-abbrev): J. Cell Biol
                Journal ID (hwp): jcb
                Journal ID (publisher-id): jcb
                Title: The Journal of Cell Biology
                Publisher: The Rockefeller University Press
                ISSN (Print): 0021-9525
                ISSN (Electronic): 1540-8140
                Publication date (Print): 2 March 2015
                Volume: 208
                Issue: 5
                Pages: 613-627
                Affiliations
                [1 ]Department of Biochemistry and Molecular Biology and [2 ]Department of Environmental Health Sciences, Johns Hopkins Bloomberg School of Public Health ; and [3 ]Department of Biological Chemistry , [4 ]Department of Dermatology , and [5 ]Department of Oncology, School of Medicine, Johns Hopkins University, MD 21205
                Author notes
                Correspondence to Pierre Coulombe: coulombe@ 123456jhu.edu
                [*]

                A. Arutyunov and E. Ilagan contributed equally to this paper.

                E. Ilagan’s present address is Dept. of Genetics and Complex Diseases, Harvard School of Public Health, MA 02115.

                Article
                Publisher ID: 201408026
                DOI: 10.1083/jcb.201408026
                PMC ID: 4347647
                PubMed ID: 25713416
                SO-VID: 4a05fba6-68ba-4f48-9061-cd8cf06c3e48
                Copyright © © 2015 Chung et al.
                License:

                This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

                History
                Date received : 7 August 2014
                Date accepted : 27 January 2015
                Categories
                Subject: Research Articles
                Subject: Article

                ScienceOpen disciplines: Cell biology
                Data availability:
                ScienceOpen disciplines: Cell biology

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