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      Rho, ROCK and actomyosin contractility in metastasis as drug targets

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          Abstract

          Metastasis is the spread of cancer cells around the body and the cause of the majority of cancer deaths. Metastasis is a very complex process in which cancer cells need to dramatically modify their cytoskeleton and cope with different environments to successfully colonize a secondary organ. In this review, we discuss recent findings pointing at Rho-ROCK or actomyosin force (or both) as major drivers of many of the steps required for metastatic success. We propose that these are important drug targets that need to be considered in the clinic to palliate metastatic disease.

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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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            Tumor metastasis: molecular insights and evolving paradigms.

            Scott Valastyan, Robert A Weinberg (2011)
            Metastases represent the end products of a multistep cell-biological process termed the invasion-metastasis cascade, which involves dissemination of cancer cells to anatomically distant organ sites and their subsequent adaptation to foreign tissue microenvironments. Each of these events is driven by the acquisition of genetic and/or epigenetic alterations within tumor cells and the co-option of nonneoplastic stromal cells, which together endow incipient metastatic cells with traits needed to generate macroscopic metastases. Recent advances provide provocative insights into these cell-biological and molecular changes, which have implications regarding the steps of the invasion-metastasis cascade that appear amenable to therapeutic targeting. Copyright © 2011 Elsevier Inc. All rights reserved.
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              The metastatic niche: adapting the foreign soil.

              Bethan Psaila, David Lyden (2009)
              The 'seed and soil' hypothesis for metastasis sets forth the concept that a conducive microenvironment, or niche, is required for disseminating tumour cells to engraft distant sites. This Opinion presents emerging data that support this concept and outlines the potential mechanism and temporal sequence by which changes occur in tissues distant from the primary tumour. To enable improvements in the prognosis of advanced malignancy, early interventions that target both the disseminating seed and the metastatic soil are likely to be required.
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                Author and article information

                Journal
                Journal ID (nlm-ta): F1000Res
                Journal ID (iso-abbrev): F1000Res
                Journal ID (pmc): F1000Research
                Title: F1000Research
                Publisher: F1000Research (London, UK )
                ISSN (Electronic): 2046-1402
                Publication date (Electronic): 29 April 2016
                Publication date Collection: 2016
                Volume: 5
                Electronic Location Identifier: F1000 Faculty Rev-783
                Affiliations
                [1 ]Tumour Plasticity Laboratory, Randall Division of Cell and Molecular Biophysics, Guy’s Campus, King’s College London, London, SE1 1UL, UK
                [2 ]Department of Imaging Chemistry and Biology, Division of Imaging Sciences and Biomedical Engineering, St. Thomas Hospital, King’s College London, London, SE1 7EH, UK
                Author notes

                #Contributed equally

                Competing interests: The authors declare that they have no competing interests.

                Article
                DOI: 10.12688/f1000research.7909.1
                PMC ID: 4856114
                PubMed ID: 27158478
                SO-VID: 1b6d4364-4b7a-4be0-859e-0613ff569443
                Copyright © Copyright: © 2016 Rodriguez-Hernandez I et al.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution Licence, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date accepted : 26 April 2016
                Funding
                Funded by: Cancer Research UK
                Award ID: C33043/A12065
                Funded by: Royal Society
                Award ID: RG110591
                Funded by: Medical Research Council
                Award ID: C97993H
                This work was supported by Cancer Research UK C33043/A12065 (Victoria Sanz-Moreno and Irene Rodriguez-Hernandez) and Royal Society RG110591 (Victoria Sanz-Moreno). Irene Rodriguez-Hernandez is supported by Fundacion Alfonso Martin Escudero, Gaia Cantelli by the Medical Research Council (C97993H), and Bruce Fanshawe by the King’s Bioscience Institute and the Guy’s and St Thomas’ Charity Prize PhD Program in Biomedical and Translational Science.
                The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Subject: Review
                Subject: Articles
                Subject: Cancer Therapeutics
                Subject: Cell Adhesion
                Subject: Cell Growth & Division
                Subject: Cell Signaling
                Subject: Cytoskeleton
                Subject: Drug Discovery & Design
                Subject: Membranes & Sorting

                Keywords: rho-rock,actomyosin,metastasis,rho
                Data availability:
                Keywords: rho-rock, actomyosin, metastasis, rho

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