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      Exosomes: composition, biogenesis, and mechanisms in cancer metastasis and drug resistance

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          Abstract

          Tumor-derived exosomes (TDEs) participate in formation and progression of different cancer processes, including tumor microenvironment (TME) remodeling, angiogenesis, invasion, metastasis and drug-resistance. Exosomes initiate or suppress various signaling pathways in the recipient cells via transmitting heterogeneous cargoes. In this review we discuss exosome biogenesis, exosome mediated metastasis and chemoresistance. Furthermore, tumor derived exosomes role in tumor microenvironment remodeling, and angiogenesis is reviewed. Also, exosome induction of epithelial mesenchymal transition (EMT) is highlighted. More importantly, we discuss extensively how exosomes regulate drug resistance in several cancers. Thus, understanding exosome biogenesis, their contents and the molecular mechanisms and signaling pathways that are responsible for metastasis and drug-resistance mediated by TDEs may help to devise novel therapeutic approaches for cancer progression particularly to overcome therapy-resistance and preventing metastasis as major factors of cancer mortality.

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          The online version of this article (10.1186/s12943-019-0991-5) contains supplementary material, which is available to authorized users.

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          Role of the vascular endothelial growth factor pathway in tumor growth and angiogenesis.

          Daniel Hicklin, Lee Ellis (2005)
          New blood vessel formation (angiogenesis) is a fundamental event in the process of tumor growth and metastatic dissemination. Hence, the molecular basis of tumor angiogenesis has been of keen interest in the field of cancer research. The vascular endothelial growth factor (VEGF) pathway is well established as one of the key regulators of this process. The VEGF/VEGF-receptor axis is composed of multiple ligands and receptors with overlapping and distinct ligand-receptor binding specificities, cell-type expression, and function. Activation of the VEGF-receptor pathway triggers a network of signaling processes that promote endothelial cell growth, migration, and survival from pre-existing vasculature. In addition, VEGF mediates vessel permeability, and has been associated with malignant effusions. More recently, an important role for VEGF has emerged in mobilization of endothelial progenitor cells from the bone marrow to distant sites of neovascularization. The well-established role of VEGF in promoting tumor angiogenesis and the pathogenesis of human cancers has led to the rational design and development of agents that selectively target this pathway. Studies with various anti-VEGF/VEGF-receptor therapies have shown that these agents can potently inhibit angiogenesis and tumor growth in preclinical models. Recently, an anti-VEGF antibody (bevacizumab), when used in combination with chemotherapy, was shown to significantly improve survival and response rates in patients with metastatic colorectal cancer and thus, validate VEGF pathway inhibitors as an important new treatment modality in cancer therapy.
          Article 0 comments Cited 639 times – based on 0 reviews     Review now
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            Exosomes: a common pathway for a specialized function.

            Guillaume van Niel, Isabel Porto-Carreiro, Sabrina Simões … (2006)
            Exosomes are membrane vesicles that are released by cells upon fusion of multivesicular bodies with the plasma membrane. Their molecular composition reflects their origin in endosomes as intraluminal vesicles. In addition to a common set of membrane and cytosolic molecules, exosomes harbor unique subsets of proteins linked to cell type-associated functions. Exosome secretion participates in the eradication of obsolete proteins but several findings, essentially in the immune system, indicate that exosomes constitute a potential mode of intercellular communication. Release of exosomes by tumor cells and their implication in the propagation of unconventional pathogens such as prions suggests their participation in pathological situations. These findings open up new therapeutic and diagnostic strategies.
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              Targeting Epithelial–Mesenchymal Transition (EMT) to Overcome Drug Resistance in Cancer

              Bowen Du, Joong Sup Shim (2016)
              Epithelial–mesenchymal transition (EMT) is known to play an important role in cancer progression, metastasis and drug resistance. Although there are controversies surrounding the causal relationship between EMT and cancer metastasis, the role of EMT in cancer drug resistance has been increasingly recognized. Numerous EMT-related signaling pathways are involved in drug resistance in cancer cells. Cells undergoing EMT show a feature similar to cancer stem cells (CSCs), such as an increase in drug efflux pumps and anti-apoptotic effects. Therefore, targeting EMT has been considered a novel opportunity to overcome cancer drug resistance. This review describes the mechanism by which EMT contributes to drug resistance in cancer cells and summarizes new advances in research in EMT-associated drug resistance.
              Article 0 comments Cited 318 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Suresh K. Alahari: 504-568-4734 , salaha@lsuhsc.edu
                Journal
                Journal ID (nlm-ta): Mol Cancer
                Journal ID (iso-abbrev): Mol. Cancer
                Title: Molecular Cancer
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1476-4598
                Publication date (Electronic): 2 April 2019
                Publication date PMC-release: 2 April 2019
                Publication date Collection: 2019
                Volume: 18
                Electronic Location Identifier: 75
                Affiliations
                [1 ]ISNI 0000 0004 0382 5622, GRID grid.440800.8, Department of Genetics, Faculty of Science, , Shahrekord University, ; Shahrekord, Iran
                [2 ]ISNI 0000 0000 8954 1233, GRID grid.279863.1, Department of Biochemistry and Molecular Biology, LSUHSC School of Medicine, ; New Orleans, USA
                [3 ]Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115 USA
                [4 ]ISNI 0000 0001 2198 6209, GRID grid.411583.a, Medical Genetics Research Center, , Mashhad University of Medical Sciences, ; Mashhad, Iran
                Article
                Publisher ID: 991
                DOI: 10.1186/s12943-019-0991-5
                PMC ID: 6444571
                PubMed ID: 30940145
                SO-VID: b8e2ecaa-589a-420b-a5d4-d3af9139245f
                Copyright © © The Author(s). 2019
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Date received : 20 November 2018
                Date accepted : 27 February 2019
                Categories
                Subject: Review
                Custom metadata
                issue-copyright-statement © The Author(s) 2019

                ScienceOpen disciplines: Oncology & Radiotherapy
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy

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