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      Clinical relevance of circulating MACC1 and S100A4 transcripts for ovarian cancer

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          Abstract

          Metastasis‐associated in colon cancer 1 ( MACC1) and S100 calcium‐binding protein A4 (S100A4) are prominent inducers of tumor progression and metastasis. For the first time, we systematically tracked circulating serum levels of MACC1 and S100A4 transcripts in the course of surgery and chemotherapy and analyzed their clinical relevance for ovarian cancer. MACC1 and S100A4 transcripts were quantified in a total of 318 serum samples from 79 ovarian cancer patients by RT‐ qPCR and digital droplet PCR, respectively. MACC1 and S100A4 transcripts were significantly elevated in serum of ovarian cancer patients, compared to healthy controls ( P = 0.024; P < 0.001). At primary diagnosis, high levels of MACC1 or S100A4 correlated with advanced FIGO stage ( P = 0.042; P = 0.008), predicted suboptimal debulking surgery and indicated shorter progression‐free survival ( PFS; P = 0.003; P = 0.001) and overall survival ( OS; P = 0.001; P = 0.002). This is the first study in ovarian cancer to propose circulating MACC1 and S100A4 transcripts as potential liquid biopsy markers.

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          S100 proteins in cancer.

          Anne Bresnick, David Weber, Danna B Zimmer (2015)
          In humans, the S100 protein family is composed of 21 members that exhibit a high degree of structural similarity, but are not functionally interchangeable. This family of proteins modulates cellular responses by functioning both as intracellular Ca(2+) sensors and as extracellular factors. Dysregulated expression of multiple members of the S100 family is a common feature of human cancers, with each type of cancer showing a unique S100 protein profile or signature. Emerging in vivo evidence indicates that the biology of most S100 proteins is complex and multifactorial, and that these proteins actively contribute to tumorigenic processes such as cell proliferation, metastasis, angiogenesis and immune evasion. Drug discovery efforts have identified leads for inhibiting several S100 family members, and two of the identified inhibitors have progressed to clinical trials in patients with cancer. This Review highlights new findings regarding the role of S100 family members in cancer diagnosis and treatment, the contribution of S100 signalling to tumour biology, and the discovery and development of S100 inhibitors for treating cancer.
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            Functions of S100 proteins.

            R. DONATO, B Cannon, G Sorci … (2013)
            The S100 protein family consists of 24 members functionally distributed into three main subgroups: those that only exert intracellular regulatory effects, those with intracellular and extracellular functions and those which mainly exert extracellular regulatory effects. S100 proteins are only expressed in vertebrates and show cell-specific expression patterns. In some instances, a particular S100 protein can be induced in pathological circumstances in a cell type that does not express it in normal physiological conditions. Within cells, S100 proteins are involved in aspects of regulation of proliferation, differentiation, apoptosis, Ca2+ homeostasis, energy metabolism, inflammation and migration/invasion through interactions with a variety of target proteins including enzymes, cytoskeletal subunits, receptors, transcription factors and nucleic acids. Some S100 proteins are secreted or released and regulate cell functions in an autocrine and paracrine manner via activation of surface receptors (e.g. the receptor for advanced glycation end-products and toll-like receptor 4), G-protein-coupled receptors, scavenger receptors, or heparan sulfate proteoglycans and N-glycans. Extracellular S100A4 and S100B also interact with epidermal growth factor and basic fibroblast growth factor, respectively, thereby enhancing the activity of the corresponding receptors. Thus, extracellular S100 proteins exert regulatory activities on monocytes/macrophages/microglia, neutrophils, lymphocytes, mast cells, articular chondrocytes, endothelial and vascular smooth muscle cells, neurons, astrocytes, Schwann cells, epithelial cells, myoblasts and cardiomyocytes, thereby participating in innate and adaptive immune responses, cell migration and chemotaxis, tissue development and repair, and leukocyte and tumor cell invasion.
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              MACC1, a newly identified key regulator of HGF-MET signaling, predicts colon cancer metastasis.

              Ulrike Stein, Wolfgang Walther, Franziska Arlt … (2009)
              We identified a previously undescribed gene associated with colon cancer by genome-wide expression analysis in primary and metastatic carcinomas: metastasis-associated in colon cancer-1, MACC1. MACC1 expression in tumor specimens is an independent prognostic indicator of metastasis formation and metastasis-free survival. We show that the gene encoding the hepatocyte growth factor (HGF) receptor, MET, is a transcriptional target of MACC1. MACC1 promotes proliferation, invasion and HGF-induced scattering of colon cancer cells in cell culture and tumor growth and metastasis in mouse models. These phenotypes are lost in cells expressing MACC1 mutants lacking the SH3 domain or the proline-rich motif. For clinical practice, MACC1 will be useful for the identification of poor prognosis subjects with colorectal cancer and is a promising new target for intervention in metastasis formation.
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                Author and article information

                Contributors
                Jan Dominik Kuhlmann: jan.kuhlmann@uniklinikum-dresden.de
                Ulrike Stein: ustein@mdc-berlin.de
                Journal
                Journal ID (nlm-ta): Mol Oncol
                Journal ID (iso-abbrev): Mol Oncol
                Journal ID (doi): 10.1002/(ISSN)1878-0261
                Journal ID (publisher-id): MOL2
                Title: Molecular Oncology
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Print): 1574-7891
                ISSN (Electronic): 1878-0261
                Publication date (Electronic): 15 April 2019
                Publication date (Print): May 2019
                Volume: 13
                Issue: 5 ( doiID: 10.1002/mol2.2019.13.issue-5 )
                Pages: 1268-1279
                Affiliations
                [ 1 ] Department of Gynecology and Obstetrics Medical Faculty University Hospital Carl Gustav Carus Technische Universität Dresden Germany
                [ 2 ] National Center for Tumor Diseases (NCT), Dresden, Germany; German Cancer Research Center (DKFZ), Heidelberg, Germany; Faculty of Medicine and University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany; Helmholtz‐Zentrum Dresden – Rossendorf (HZDR) Dresden Germany
                [ 3 ] German Cancer Consortium (DKTK) Dresden and German Cancer Research Center (DKFZ) Heidelberg Germany
                [ 4 ] Experimental and Clinical Research Center Charité – Universitätsmedizin Berlinand Max‐Delbrück‐Center for Molecular Medicine in the Helmholtz Association Berlin Germany
                [ 5 ] German Cancer Consortium (DKTK) Berlin and German Cancer Research Center (DKFZ) Heidelberg Germany
                [ 6 ] Medizinische Klinik und Poliklinik I Medical Faculty and University Hospital Technische Universität Dresden Germany
                [ 7 ] DRK‐Blood Donor Service ITM Plauen Germany
                Author notes
                [*] [* ] Correspondence

                J. D. Kuhlmann, Department of Gynecology and Obstetrics, Technische Universität Dresden, Fetscherstraße 74, D‐01307 Dresden, Germany

                Fax: +49 351 458 5844

                Tel: +49 351 458 2434

                E‐mail: jan.kuhlmann@ 123456uniklinikum-dresden.de

                and

                U. Stein, Experimental and Clinical Research Center, Charité – Universitätsmedizin Berlin and Max‐Delbrück‐Center for Molecular Medicine in the Helmholtz Association, Department of Translational Oncology of Solid Tumors, Robert‐Rössle‐Straße 10, D‐13125 Berlin, Germany

                Fax: +49 30 94062780

                Tel: +49 30 94063432

                E‐mail: ustein@ 123456mdc-berlin.de

                Article
                Publisher ID: MOL212484
                DOI: 10.1002/1878-0261.12484
                PMC ID: 6487687
                PubMed ID: 30927479
                SO-VID: 412521a7-d2b3-4494-8fd7-3e5d04997d12
                Copyright © © 2019 The Authors. Published by FEBS Press and John Wiley & Sons Ltd.
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 31 October 2018
                Date accepted : 29 March 2019
                Page count
                Figures: 5, Tables: 1, Pages: 12, Words: 6967
                Funding
                Funded by: German Cancer Consortium
                Award ID: DKTK
                Categories
                Subject: Research Article
                Subject: Research Articles
                Custom metadata
                source-schema-version-number 2.0
                component-id mol212484
                cover-date May 2019
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_NLMPMC version:5.6.2.1 mode:remove_FC converted:29.04.2019

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: blood‐based biomarker,macc1,ovarian cancer,prognosis,s100a4,survival
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: blood‐based biomarker, macc1, ovarian cancer, prognosis, s100a4, survival

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