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      From Plasminogen to Plasmin: Role of Plasminogen Receptors in Human Cancer

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          Abstract

          Cell surface-associated proteolysis mediated by plasmin (PLA) is an essential feature of wound healing, angiogenesis and cell invasion, processes that are dysregulated in cancer development, progression and systemic spread. The generation of PLA, initiated by the binding of its precursor plasminogen (PLG) to the cell surface, is regulated by an array of activators, inhibitors and receptors. In this review, we will highlight the importance of the best-characterized components of the PLG/PLA cascade in the pathogenesis of cancer focusing on the role of the cell surface-PLG receptors (PLG-R). PLG-R overexpression has been associated with poor prognosis of cancer patients and resistance to chemotherapy. We will also discuss recent findings on the molecular mechanisms regulating cell surface expression and distribution of PLG-R.

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          Cancer statistics, 2006.

          Ahmedin Jemal, Rebecca Siegel, Elizabeth Ward … (2006)
          Each year, the American Cancer Society estimates the number of new cancer cases and deaths expected in the United States in the current year and compiles the most recent data on cancer incidence, mortality, and survival based on incidence data from the National Cancer Institute and mortality data from the National Center for Health Statistics. Incidence and death rates are age-standardized to the 2000 US standard million population. A total of 1,399,790 new cancer cases and 564,830 deaths from cancer are expected in the United States in 2006. When deaths are aggregated by age, cancer has surpassed heart disease as the leading cause of death for those younger than age 85 since 1999. Delay-adjusted cancer incidence rates stabilized in men from 1995 through 2002, but continued to increase by 0.3% per year from 1987 through 2002 in women. Between 2002 and 2003, the actual number of recorded cancer deaths decreased by 778 in men, but increased by 409 in women, resulting in a net decrease of 369, the first decrease in the total number of cancer deaths since national mortality record keeping was instituted in 1930. The death rate from all cancers combined has decreased by 1.5% per year since 1993 among men and by 0.8% per year since 1992 among women. The mortality rate has also continued to decrease for the three most common cancer sites in men (lung and bronchus, colon and rectum, and prostate) and for breast and colon and rectum cancers in women. Lung cancer mortality among women continues to increase slightly. In analyses by race and ethnicity, African American men and women have 40% and 18% higher death rates from all cancers combined than White men and women, respectively. Cancer incidence and death rates are lower in other racial and ethnic groups than in Whites and African Americans for all sites combined and for the four major cancer sites. However, these groups generally have higher rates for stomach, liver, and cervical cancers than Whites. Furthermore, minority populations are more likely to be diagnosed with advanced stage disease than are Whites. Progress in reducing the burden of suffering and death from cancer can be accelerated by applying existing cancer control knowledge across all segments of the population.
          Article 0 comments Cited 486 times – based on 0 reviews     Review now
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            The roles of IFN gamma in protection against tumor development and cancer immunoediting.

            Hiroaki Ikeda, Lloyd Old, Robert Schreiber (2002)
            Interferon-gamma (IFN gamma) is a cytokine that plays physiologically important roles in promoting innate and adaptive immune responses. The absence of IFN gamma production or cellular responsiveness in humans and experimental animals significantly predisposes the host to microbial infection, a result that validates the physiologic importance of this cytokine in preventing infectious disease. Recently, an additional role for IFN gamma in preventing development of primary and transplanted tumors has been identified. Although there now appears to be a consensus that IFN gamma promotes host responses to tumors, the mechanisms by which this cytokine achieves its effects remain unclear. In this review, we briefly discuss key issues of the molecular cell biology of IFN gamma and its receptor that are most relevant to IFN gamma-dependent anti-tumor effects and then focus on the data implicating IFN gamma as a critical immune system component that regulates tumor development. Potential mechanisms underlying IFN gamma's anti-tumor effects are discussed and a preliminary integrative model of IFN gamma's actions on tumors is proposed. Finally, the capacity of IFN gamma and lymphocytes to not only provide protection against tumor development but also to sculpt the immunogenic phenotype of tumors that develop in an immunocompetent host is presented and introduced as a "cancer immunoediting" process.
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              The lamellipodium: where motility begins

              J.Victor Small, Theresia Stradal, Emmanuel Vignal … (2002)
              Lamellipodia, filopodia and membrane ruffles are essential for cell motility, the organization of membrane domains, phagocytosis and the development of substrate adhesions. Their formation relies on the regulated recruitment of molecular scaffolds to their tips (to harness and localize actin polymerization), coupled to the coordinated organization of actin filaments into lamella networks and bundled arrays. Their turnover requires further molecular complexes for the disassembly and recycling of lamellipodium components. Here, we give a spatial inventory of the many molecular players in this dynamic domain of the actin cytoskeleton in order to highlight the open questions and the challenges ahead.
              Article 0 comments Cited 186 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                William Chi-shing Cho: Role: External Editor
                Journal
                Journal ID (nlm-ta): Int J Mol Sci
                Journal ID (iso-abbrev): Int J Mol Sci
                Journal ID (publisher-id): ijms
                Title: International Journal of Molecular Sciences
                Publisher: MDPI
                ISSN (Electronic): 1422-0067
                Publication date (Electronic): 17 November 2014
                Publication date Collection: November 2014
                Volume: 15
                Issue: 11
                Pages: 21229-21252
                Affiliations
                [1 ]Department of Biochemistry, Faculty of Medicine, University of Giessen Lung Center, Friedrichstrasse 24, 35392 Giessen, Germany; E-Mails: miroslava.didiasova@ 123456biochemie.med.uni-giessen.de (M.D.); lukasz.wujak@ 123456mpi-bn.mpg.de (L.W.)
                [2 ]The German Center for Lung Research, 35392 Giessen, Germany; E-Mail: malgorzata.wygrecka@ 123456innere.med.uni-giessen.de
                Author notes
                [†]

                These authors contributed equally to this work.

                [* ]Author to whom correspondence should be addressed; E-Mail: dariusz.zakrzewicz@ 123456innere.med.uni-giessen.de ; Tel.: +49-641-99-47508; Fax: +49-641-99-47509.
                Article
                Publisher ID: ijms-15-21229
                DOI: 10.3390/ijms151121229
                PMC ID: 4264222
                PubMed ID: 25407528
                SO-VID: a5cbf2ef-32a4-4667-8303-ae63eecafa39
                Copyright © © 2014 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 Attribution license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 27 August 2014
                Date revision received : 04 November 2014
                Date accepted : 12 November 2014
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular biology
                Keywords: actin,annexin 2,cytokeratin-8,enolase-1,plasmin,plasminogen,plasminogen receptor
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: actin, annexin 2, cytokeratin-8, enolase-1, plasmin, plasminogen, plasminogen receptor

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