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      ADAM9 promotes lung cancer progression through vascular remodeling by VEGFA, ANGPT2, and PLAT

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          Abstract

          Lung cancer has a very high prevalence of brain metastasis, which results in a poor clinical outcome. Up-regulation of a disintegrin and metalloproteinase 9 (ADAM9) in lung cancer cells is correlated with metastasis to the brain. However, the molecular mechanism underlying this correlation remains to be elucidated. Since angiogenesis is an essential step for brain metastasis, microarray experiments were used to explore ADAM9-regulated genes that function in vascular remodeling. The results showed that the expression levels of vascular endothelial growth factor A (VEGFA), angiopoietin-2 (ANGPT2), and tissue plasminogen activator (PLAT) were suppressed in ADAM9-silenced cells, which in turn leads to decreases in angiogenesis, vascular remodeling, and tumor growth in vivo. Furthermore, simultaneous high expression of ADAM9 and VEGFA or of ADAM9 and ANGPT2 was correlated with poor prognosis in a clinical dataset. These findings suggest that ADAM9 promotes tumorigenesis through vascular remodeling, particularly by increasing the function of VEGFA, ANGPT2, and PLAT.

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          Gene expression-based survival prediction in lung adenocarcinoma: a multi-site, blinded validation study.

          Kerby Shedden, Jeremy M. G. Taylor, Steven A. Enkemann … (2008)
          Although prognostic gene expression signatures for survival in early-stage lung cancer have been proposed, for clinical application, it is critical to establish their performance across different subject populations and in different laboratories. Here we report a large, training-testing, multi-site, blinded validation study to characterize the performance of several prognostic models based on gene expression for 442 lung adenocarcinomas. The hypotheses proposed examined whether microarray measurements of gene expression either alone or combined with basic clinical covariates (stage, age, sex) could be used to predict overall survival in lung cancer subjects. Several models examined produced risk scores that substantially correlated with actual subject outcome. Most methods performed better with clinical data, supporting the combined use of clinical and molecular information when building prognostic models for early-stage lung cancer. This study also provides the largest available set of microarray data with extensive pathological and clinical annotation for lung adenocarcinomas.
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            Real-time imaging reveals the single steps of brain metastasis formation.

            Yvonne Kienast, Louisa von Baumgarten, Martin Fuhrmann … (2010)
            Brain metastasis frequently occurs in individuals with cancer and is often fatal. We used multiphoton laser scanning microscopy to image the single steps of metastasis formation in real time. Thus, it was possible to track the fate of individual metastasizing cancer cells in vivo in relation to blood vessels deep in the mouse brain over minutes to months. The essential steps in this model were arrest at vascular branch points, early extravasation, persistent close contacts to microvessels and perivascular growth by vessel cooption (melanoma) or early angiogenesis (lung cancer). Inefficient steps differed between the tumor types. Long-term dormancy was only observed for single perivascular cancer cells, some of which moved continuously. Vascular endothelial growth factor-A (VEGF-A) inhibition induced long-term dormancy of lung cancer micrometastases by preventing angiogenic growth to macrometastases. The ability to image the establishment of brain metastases in vivo provides new insights into their evolution and response to therapies.
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              Brain metastases: epidemiology and pathophysiology.

              Igor Gavrilovic, Jerome Posner (2005)
              Metastases are the most common tumors of the central nervous system (CNS), but cancer databases are often incomplete leading to underestimation of the incidence of even symptomatic brain metastases. Brain imaging studies are not routinely performed on neurologically asymptomatic cancer patients and autopsy studies are outdated. Furthermore, while incidence rates for cancers are stable and mortality is decreasing due to earlier detection and better therapy, the incidence of brain metastases appears to be increasing. The pathophysiology of brain metastases is a complex multistage process, mediated by molecular mechanisms; from the primary organ, cancer cells must transform, grow and be transported to the CNS where they can lay dormant for various lengths of time before invading and growing further. Understanding the pathophysiology of brain metastases is of great importance, because it may lead to the development of more efficient therapies to combat brain tumor growth or to possibly make the CNS an undesirable environment for tumor progression.
              Article 0 comments Cited 247 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Yuh-Pyng Sher: ypsher@mail.cmu.edu.tw
                Journal
                Journal ID (nlm-ta): Sci Rep
                Journal ID (iso-abbrev): Sci Rep
                Title: Scientific Reports
                Publisher: Nature Publishing Group UK (London )
                ISSN (Electronic): 2045-2322
                Publication date (Electronic): 8 November 2017
                Publication date PMC-release: 8 November 2017
                Publication date Collection: 2017
                Volume: 7
                Electronic Location Identifier: 15108
                Affiliations
                [1 ]ISNI 0000 0001 0083 6092, GRID grid.254145.3, Graduate Institute of Clinical Medical Science, China Medical University, ; Taichung, 404 Taiwan
                [2 ]ISNI 0000 0001 0083 6092, GRID grid.254145.3, Graduate Institute of Biomedical Sciences, China Medical University, ; Taichung, 404 Taiwan
                [3 ]ISNI 0000 0001 0083 6092, GRID grid.254145.3, Department of Biomedical Imaging and Radiological Science, China Medical University, ; Taichung, 404 Taiwan
                [4 ]ISNI 0000 0004 0572 9415, GRID grid.411508.9, Center for Molecular Medicine, China Medical University Hospital, ; Taichung, 404 Taiwan
                [5 ]ISNI 0000 0004 0572 9415, GRID grid.411508.9, Division of Hematology and Oncology, China Medical University Hospital, ; Taichung, 404 Taiwan
                [6 ]ISNI 0000 0004 0572 9415, GRID grid.411508.9, Division of Thoracic Surgery, China Medical University Hospital, ; Taichung, 404 Taiwan
                [7 ]ISNI 0000 0004 0572 9415, GRID grid.411508.9, Department of Radiation Oncology, , China Medical University Hospital, ; Taichung, 404 Taiwan
                [8 ]ISNI 0000 0004 0546 0241, GRID grid.19188.39, Graduate Institute of Physiology, National Taiwan University, ; Taipei, 106 Taiwan
                [9 ]ISNI 0000 0004 0546 0241, GRID grid.19188.39, Department of Public Health, National Taiwan University, ; Taipei, 106 Taiwan
                Author information
                http://orcid.org/0000-0002-3913-5338
                Article
                Publisher ID: 15159
                DOI: 10.1038/s41598-017-15159-1
                PMC ID: 5678093
                PubMed ID: 29118335
                SO-VID: da4c412b-055e-41b8-b31a-90a7cda3da1d
                Copyright © © The Author(s) 2017
                License:

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 17 February 2017
                Date accepted : 23 October 2017
                Categories
                Subject: Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2017

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