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      Exploring the Role of RGD-Recognizing Integrins in Cancer

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          Abstract

          Integrins are key regulators of communication between cells and with their microenvironment. Eight members of the integrin superfamily recognize the tripeptide motif Arg-Gly-Asp (RGD) within extracelluar matrix (ECM) proteins. These integrins constitute an important subfamily and play a major role in cancer progression and metastasis via their tumor biological functions. Such transmembrane adhesion and signaling receptors are thus recognized as promising and well accessible targets for novel diagnostic and therapeutic applications for directly attacking cancer cells and their fatal microenvironment. Recently, specific small peptidic and peptidomimetic ligands as well as antibodies binding to distinct integrin subtypes have been developed and synthesized as new drug candidates for cancer treatment. Understanding the distinct functions and interplay of integrin subtypes is a prerequisite for selective intervention in integrin-mediated diseases. Integrin subtype-specific ligands labelled with radioisotopes or fluorescent molecules allows the characterization of the integrin patterns in vivo and later the medical intervention via subtype specific drugs. The coating of nanoparticles, larger proteins, or encapsulating agents by integrin ligands are being explored to guide cytotoxic reagents directly to the cancer cell surface. These ligands are currently under investigation in clinical studies for their efficacy in interference with tumor cell adhesion, migration/invasion, proliferation, signaling, and survival, opening new treatment approaches in personalized medicine.

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          Most cited references238

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          Latent TGF-β structure and activation.

          Transforming growth factor (TGF)-β is stored in the extracellular matrix as a latent complex with its prodomain. Activation of TGF-β1 requires the binding of α(v) integrin to an RGD sequence in the prodomain and exertion of force on this domain, which is held in the extracellular matrix by latent TGF-β binding proteins. Crystals of dimeric porcine proTGF-β1 reveal a ring-shaped complex, a novel fold for the prodomain, and show how the prodomain shields the growth factor from recognition by receptors and alters its conformation. Complex formation between α(v)β(6) integrin and the prodomain is insufficient for TGF-β1 release. Force-dependent activation requires unfastening of a 'straitjacket' that encircles each growth-factor monomer at a position that can be locked by a disulphide bond. Sequences of all 33 TGF-β family members indicate a similar prodomain fold. The structure provides insights into the regulation of a family of growth and differentiation factors of fundamental importance in morphogenesis and homeostasis.
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            Crystal structure of the extracellular segment of integrin alpha Vbeta3 in complex with an Arg-Gly-Asp ligand.

            The structural basis for the divalent cation-dependent binding of heterodimeric alphabeta integrins to their ligands, which contain the prototypical Arg-Gly-Asp sequence, is unknown. Interaction with ligands triggers tertiary and quaternary structural rearrangements in integrins that are needed for cell signaling. Here we report the crystal structure of the extracellular segment of integrin alphaVbeta3 in complex with a cyclic peptide presenting the Arg-Gly-Asp sequence. The ligand binds at the major interface between the alphaV and beta3 subunits and makes extensive contacts with both. Both tertiary and quaternary changes are observed in the presence of ligand. The tertiary rearrangements take place in betaA, the ligand-binding domain of beta3; in the complex, betaA acquires two cations, one of which contacts the ligand Asp directly and the other stabilizes the ligand-binding surface. Ligand binding induces small changes in the orientation of alphaV relative to beta3.
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              Adhesion signaling - crosstalk between integrins, Src and Rho.

              Interactions between cells and the extracellular matrix coordinate signaling pathways that control various aspects of cellular behavior. Integrins sense the physical properties of the extracellular matrix and organize the cytoskeleton accordingly. In turn, this modulates signaling pathways that are triggered by various other transmembrane receptors and augments the cellular response to growth factors. Over the past years, it has become clear that there is extensive crosstalk between integrins, Src-family kinases and Rho-family GTPases at the heart of such adhesion signaling. In this Commentary, we discuss recent advances in our understanding of the dynamic regulation of the molecular connections between these three protein families. We also discuss how this signaling network can regulate a range of cellular processes that are important for normal tissue function and disease, including cell adhesion, spreading, migration and mechanotransduction.
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                Author and article information

                Contributors
                Role: Academic Editor
                Journal
                Cancers (Basel)
                Cancers (Basel)
                cancers
                Cancers
                MDPI
                2072-6694
                04 September 2017
                September 2017
                : 9
                : 9
                : 116
                Affiliations
                [1 ]Department of Oral and Maxillofacial Surgery, University Hospital Rechts der Isar, Technische Universität München, Ismaninger Straße 22, 81679 Munich, Germany
                [2 ]Clinical Research Unit, Department of Obstetrics & Gynecology, Technische Universität München, Ismaninger Straße 22, 81675 Munich, Germany; ute.reuning@ 123456mri.tum.de
                [3 ]Institute for Advanced Study and Center for Integrated Protein Science (CIPSM), Department Chemie, Technische Universität München, Lichtenbergstraße 4, 85747 Garching, Germany; florian.fr.reichart@ 123456tum.de (F.R.); michael.weinmueller@ 123456tum.de (M.W.); andreas.raeder@ 123456mytum.de (A.R.)
                [4 ]Pharmaceutical Radiochemistry, Technische Universität München, Walther-Meißner-Straße 3, 85748 Garching, Germany; johannes.notni@ 123456tum.de (J.N.); h.j.wester@ 123456tum.de (H.-J.W.)
                [5 ]Department of Nuclear Medicine, Technische Universität München, Ismaninger Straße 22, 81679 Munich, Germany; markus.schwaiger@ 123456tum.de
                [6 ]Institute of Pathology, Technische Universität München, Trogerstraße 18, 81675 Munich, Germany; katja.steiger@ 123456tum.de
                Author notes
                [* ]Correspondence: markus.nieberler@ 123456tum.de (M.N.); kessler@ 123456tum.de (H.K.); Tel.: +49-89-4140–5916 (M.N.) or +49-163-4714-383 (M.N.); Fax: +49-89-4140-4993 (M.N.)
                [†]

                These authors contributed equally to this work.

                Author information
                https://orcid.org/0000-0002-3964-3391
                https://orcid.org/0000-0002-0865-2519
                https://orcid.org/0000-0002-7269-5433
                https://orcid.org/0000-0002-7292-9789
                Article
                cancers-09-00116
                10.3390/cancers9090116
                5615331
                28869579
                8140702b-5b61-43cd-9ff1-9f0c70e00f7b
                © 2017 by the authors.

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

                History
                : 06 July 2017
                : 31 August 2017
                Categories
                Review

                rgd-recognizing integrins,αvβ3,αvβ5,αvβ6,αvβ8,α5β1,α8β1,integrin adhesion,migration,apoptosis,and signaling,synthetic integrin ligands,cyclic peptide,peptidomimetics,cilengitide,epithelial-mesenchymal transition (emt),transforming growth factor-β (tgf-β),metastasis,angiogenesis

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