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      aV integrins and TGF-β-induced EMT: a circle of regulation

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          Abstract

          Transforming growth factor-β (TGF-β) has roles in embryonic development, the prevention of inappropriate inflammation and tumour suppression. However, TGF-β signalling also regulates pathological epithelial-to-mesenchymal transition (EMT), inducing or progressing a number of diseases ranging from inflammatory disorders, to fibrosis and cancer. However, TGF-β signalling does not proceed linearly but rather induces a complex network of cascades that mutually influence each other and cross-talk with other pathways to successfully induce EMT. Particularly, there is substantial evidence for cross-talk between αV integrins and TGF-β during EMT, and anti-integrin therapeutics are under development as treatments for TGF-β-related disorders. However, TGF-β’s complex signalling network makes the development of therapeutics to block TGF-β-mediated pathology challenging. Moreover, despite our current understanding of integrins and TGF-β function during EMT, the precise mechanism of their role during physiological versus pathological EMT is not fully understood. This review focuses on the circle of regulation between αV integrin and TGF-β signalling during TGF-β induced EMT, which pose as a significant driver to many known TGF-β-mediated disorders.

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          Epithelial-mesenchymal transitions in development and disease.

          Jean Paul Thiery, Hervé Acloque, Ruby Y J Huang … (2009)
          The epithelial to mesenchymal transition (EMT) plays crucial roles in the formation of the body plan and in the differentiation of multiple tissues and organs. EMT also contributes to tissue repair, but it can adversely cause organ fibrosis and promote carcinoma progression through a variety of mechanisms. EMT endows cells with migratory and invasive properties, induces stem cell properties, prevents apoptosis and senescence, and contributes to immunosuppression. Thus, the mesenchymal state is associated with the capacity of cells to migrate to distant organs and maintain stemness, allowing their subsequent differentiation into multiple cell types during development and the initiation of metastasis.
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            RGD and other recognition sequences for integrins.

            E Ruoslahti (1996)
            Proteins that contain the Arg-Gly-Asp (RGD) attachment site, together with the integrins that serve as receptors for them, constitute a major recognition system for cell adhesion. The RGD sequence is the cell attachment site of a large number of adhesive extracellular matrix, blood, and cell surface proteins, and nearly half of the over 20 known integrins recognize this sequence in their adhesion protein ligands. Some other integrins bind to related sequences in their ligands. The integrin-binding activity of adhesion proteins can be reproduced by short synthetic peptides containing the RGD sequence. Such peptides promote cell adhesion when insolubilized onto a surface, and inhibit it when presented to cells in solution. Reagents that bind selectively to only one or a few of the RGD-directed integrins can be designed by cyclizing peptides with selected sequences around the RGD and by synthesizing RGD mimics. As the integrin-mediated cell attachment influences and regulates cell migration, growth, differentiation, and apoptosis, the RGD peptides and mimics can be used to probe integrin functions in various biological systems. Drug design based on the RGD structure may provide new treatments for diseases such as thrombosis, osteoporosis, and cancer.
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              Targeted disruption of the mouse transforming growth factor-beta 1 gene results in multifocal inflammatory disease.

              M Shull, I Ormsby, A Kier … (1992)
              Transforming growth factor-beta 1 (TGF-beta 1) is a multifunctional growth factor that has profound regulatory effects on many developmental and physiological processes. Disruption of the TGF-beta 1 gene by homologous recombination in murine embryonic stem cells enables mice to be generated that carry the disrupted allele. Animals homozygous for the mutated TGF-beta 1 allele show no gross developmental abnormalities, but about 20 days after birth they succumb to a wasting syndrome accompanied by a multifocal, mixed inflammatory cell response and tissue necrosis, leading to organ failure and death. TGF-beta 1-deficient mice may be valuable models for human immune and inflammatory disorders, including autoimmune diseases, transplant rejection and graft versus host reactions.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Cell Mol Med
                Journal ID (iso-abbrev): J. Cell. Mol. Med
                Journal ID (publisher-id): jcmm
                Title: Journal of Cellular and Molecular Medicine
                Publisher: Blackwell Publishing Ltd (Oxford, UK )
                ISSN (Print): 1582-1838
                ISSN (Electronic): 1582-4934
                Publication date (Print): March 2012
                Publication date (Electronic): 28 February 2012
                Volume: 16
                Issue: 3
                Pages: 445-455
                Affiliations
                Department of Biological Sciences, University of Delaware Newark, DE, USA
                Author notes
                *Correspondence to: Melinda K. DUNCAN, Department of Biological Sciences, Newark, DE 19716, USA. Tel.: +1-(302)-831-0533 Fax: +1-(302)-831-2281 E-mail: duncanm@ 123456udel.edu
                Article
                DOI: 10.1111/j.1582-4934.2011.01419.x
                PMC ID: 3290750
                PubMed ID: 21883891
                SO-VID: e53ced4f-6ef6-405c-b317-f87f7e9929a4
                Copyright © © 2012 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd
                History
                Date received : 22 March 2011
                Date accepted : 09 August 2011
                Categories
                Subject: Reviews

                ScienceOpen disciplines: Molecular medicine
                Keywords: emt,tgf-β mediated disorders,αv integrins
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: emt, tgf-β mediated disorders, αv integrins

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