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      Is Open Access

      Cell matrix adhesions in cancer: The proteins that form the glue

      review-article
      1 , 1
      Oncotarget
      Impact Journals LLC
      integrins, cancer, focal adhesions

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          Abstract

          The main purposes of Integrin-mediated cell contacts are to interpret bi-directional signals between the extracellular environment and intracellular proteins, as well as, anchor the cell to a matrix. Many cell adhesion molecules have been discovered with a wide spectrum of responsibilities, including recruiting, activating, elongating, and maintaining. This review will perlustrate some of the key incidences that precede focal adhesion formation. Tyrosine phosphorylation is a key signaling initiation event that leads to the recruitment of multiple proteins to focal adhesion sites. Recruitment and concentration of proteins such as Paxillin and Vinculin to Integrin clutches is necessary for focal adhesion development. The assembled networks are responsible for transmitting signals back and forth from the extracellular matrix (ECM) to Actin and its binding proteins. Cancer cells exhibit highly altered focal adhesion dynamics. This review will highlight some key discoveries in cancer cell adhesion, as well as, identify current gaps in knowledge.

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          Most cited references152

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          Cellular motility driven by assembly and disassembly of actin filaments.

          Motile cells extend a leading edge by assembling a branched network of actin filaments that produces physical force as the polymers grow beneath the plasma membrane. A core set of proteins including actin, Arp2/3 complex, profilin, capping protein, and ADF/cofilin can reconstitute the process in vitro, and mathematical models of the constituent reactions predict the rate of motion. Signaling pathways converging on WASp/Scar proteins regulate the activity of Arp2/3 complex, which mediates the initiation of new filaments as branches on preexisting filaments. After a brief spurt of growth, capping protein terminates the elongation of the filaments. After filaments have aged by hydrolysis of their bound ATP and dissociation of the gamma phosphate, ADF/cofilin proteins promote debranching and depolymerization. Profilin catalyzes the exchange of ADP for ATP, refilling the pool of ATP-actin monomers bound to profilin, ready for elongation.
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            Integrin ligands at a glance.

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              FAK-Src signalling through paxillin, ERK and MLCK regulates adhesion disassembly.

              Cell migration is a complex, highly regulated process that involves the continuous formation and disassembly of adhesions (adhesion turnover). Adhesion formation takes place at the leading edge of protrusions, whereas disassembly occurs both at the cell rear and at the base of protrusions. Despite the importance of these processes in migration, the mechanisms that regulate adhesion formation and disassembly remain largely unknown. Here we develop quantitative assays to measure the rate of incorporation of molecules into adhesions and the departure of these proteins from adhesions. Using these assays, we show that kinases and adaptor molecules, including focal adhesion kinase (FAK), Src, p130CAS, paxillin, extracellular signal-regulated kinase (ERK) and myosin light-chain kinase (MLCK) are critical for adhesion turnover at the cell front, a process central to migration.
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                Author and article information

                Journal
                Oncotarget
                Oncotarget
                Oncotarget
                ImpactJ
                Oncotarget
                Impact Journals LLC
                1949-2553
                18 July 2017
                20 April 2017
                : 8
                : 29
                : 48471-48487
                Affiliations
                1 Department of Biochemistry and Molecular Biology, Stanley S. Scott Cancer Center, Louisiana State University Health Sciences Center, New Orleans, LA, USA
                Author notes
                Correspondence to: Suresh K. Alahari, salaha@ 123456lsuhsc.edu
                Article
                17265
                10.18632/oncotarget.17265
                5564663
                28476046
                714f4add-6b3b-413a-8632-6aa0c2f3d697
                Copyright: © 2017 Maziveyi and Alahari

                This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                : 16 November 2016
                : 27 March 2017
                Categories
                Review

                Oncology & Radiotherapy
                integrins,cancer,focal adhesions
                Oncology & Radiotherapy
                integrins, cancer, focal adhesions

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