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      TGF-β Signaling in Gastrointestinal Cancers: Progress in Basic and Clinical Research

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          Abstract

          Transforming growth factor (TGF)-β superfamily proteins have many important biological functions, including regulation of tissue differentiation, cell proliferation, and migration in both normal and cancer cells. Many studies have reported that TGF-β signaling is associated with disease progression and therapeutic resistance in several cancers. Similarly, TGF-β-induced protein (TGFBI)—a downstream component of the TGF-β signaling pathway—has been shown to promote and/or inhibit cancer. Here, we review the state of basic and clinical research on the roles of TGF-β and TGFBI in gastrointestinal cancers.

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          Mechanisms of TGF-β Signaling from Cell Membrane to the Nucleus

          Yigong Shi, Joan Massagué (2003)
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            Roles of TGFbeta in metastasis.

            David Padua, Joan Massagué (2009)
            The TGFbeta signaling pathway is conserved from flies to humans and has been shown to regulate such diverse processes as cell proliferation, differentiation, motility, adhesion, organization, and programmed cell death. Both in vitro and in vivo experiments suggest that TGFbeta can utilize these varied programs to promote cancer metastasis through its effects on the tumor microenvironment, enhanced invasive properties, and inhibition of immune cell function. Recent clinical evidence demonstrating a link between TGFbeta signaling and cancer progression is fostering interest in this signaling pathway as a therapeutic target. Anti-TGFbeta therapies are currently being developed and tested in pre-clinical studies. However, targeting TGFbeta carries a substantial risk as this pathway is implicated in multiple homeostatic processes and is also known to have tumor-suppressor functions. Additionally, clinical and experimental results show that TGFbeta has diverse and often conflicting roles in tumor progression even within the same tumor types. The development of TGFbeta inhibitors for clinical use will require a deeper understanding of TGFbeta signaling, its consequences, and the contexts in which it acts.
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              Regulation of EMT by TGFβ in cancer.

              Carl-Henrik Heldin, Michael Vanlandewijck, Aristidis Moustakas (2012)
              Transforming growth factor-β (TGFβ) suppresses tumor formation since it inhibits cell growth and promotes apoptosis. However, in advanced cancers TGFβ elicits tumor promoting effects through its ability to induce epithelial-mesenchymal transition (EMT) which enhances invasiveness and metastasis; in addition, TGFβ exerts tumor promoting effects on non-malignant cells of the tumor, including suppression of immune surveillance and stimulation of angiogenesis. TGFβ promotes EMT by transcriptional and posttranscriptional regulation of a group of transcription factors that suppresses epithelial features, such as expression of components of cell junctions and polarity complexes, and enhances mesenchymal features, such as production of matrix molecules and several cytokines and growth factors that stimulate cell migration. The EMT program has certain similarities with the stem cell program. Inducers and effectors of EMT are interesting targets for the development of improved diagnosis, prognosis and therapy of cancer. Copyright © 2012 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
              Article 0 comments Cited 216 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Andrei Turtoi: Role: Academic Editor
                Journal
                Journal ID (nlm-ta): J Clin Med
                Journal ID (iso-abbrev): J Clin Med
                Journal ID (publisher-id): jcm
                Title: Journal of Clinical Medicine
                Publisher: MDPI
                ISSN (Electronic): 2077-0383
                Publication date (Electronic): 18 January 2017
                Publication date Collection: January 2017
                Volume: 6
                Issue: 1
                Electronic Location Identifier: 11
                Affiliations
                [1 ]Research Program for Omics-based Medical Science, Division of Integrated Oncology Research, Gunma University Initiative for Advanced Research, 3-39-22 Showa-machi, Maebashi, Gunma 371-8511, Japan; m.nishiyama@ 123456gunma-u.ac.jp
                [2 ]Department of Molecular Pharmacology and Oncology, Gunma University Graduate School of Medicine, 3-39-22 Showa-machi, Maebashi, Gunma 371-8511, Japan
                Author notes
                [* ]Correspondence: bori45@ 123456gunma-u.ac.jp ; Tel.: +81-27-220-7962; Fax: +81-27-220-7963
                Article
                Publisher ID: jcm-06-00011
                DOI: 10.3390/jcm6010011
                PMC ID: 5294964
                PubMed ID: 28106769
                SO-VID: 927e8310-e98a-4740-855a-5b49b3d5f79c
                Copyright © © 2017 by the author; licensee MDPI, Basel, Switzerland.
                License:

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC-BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 17 October 2016
                Date accepted : 16 January 2017
                Categories
                Subject: Review

                Keywords: tgf-β signaling,tgfbi,gastrointestinal cancer,emt,tumor promoter,tumor suppressor
                Data availability:
                Keywords: tgf-β signaling, tgfbi, gastrointestinal cancer, emt, tumor promoter, tumor suppressor

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