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      Epithelial‐to‐mesenchymal transition transcription factors in cancer‐associated fibroblasts

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          Abstract

          Beyond inducing epithelial‐to‐mesenchymal transcription ( EMT), transcriptional factors of the Snail, ZEB and Twist families ( EMT‐ TFs) control global plasticity programmes affecting cell stemness and fate. Literature addressing the reactivation of these factors in adult tumour cells is very extensive, as they enable cancer cell plasticity and fuel both tumour initiation and metastatic spread. Incipient data reveal that EMT‐ TFs are also expressed in fibroblasts, providing these with additional properties. Here, I will review recent reports on the expression of EMT‐ TFs in cancer‐associated fibroblasts ( CAFs). The new model suggests that EMT‐ TFs can be envisioned as essential metastasis and chemoresistance‐promoting molecules, thereby enabling coordinated plasticity programmes in parenchyma and stroma–tumour compartments.

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          Molecular genetics of colorectal cancer.

          Eric R. Fearon (2011)
          Over the past three decades, molecular genetic studies have revealed some critical mutations underlying the pathogenesis of the sporadic and inherited forms of colorectal cancer (CRC). A relatively limited number of oncogenes and tumor-suppressor genes-most prominently the APC, KRAS, and p53 genes-are mutated in a sizeable fraction of CRCs, and a larger collection of genes that are mutated in subsets of CRC have begun to be defined. Together with DNA-methylation and chromatin-structure changes, the mutations act to dysregulate conserved signaling networks that exert context-dependent effects on critical cell phenotypes, including the regulation of cellular metabolism, proliferation, differentiation, and survival. Much work remains to be done to fully understand the nature and significance of the individual and collective genetic and epigenetic defects in CRC. Some key concepts for the field have emerged, two of which are emphasized in this review. Specifically, the gene defects in CRC often target proteins and pathways that exert pleiotropic effects on the cancer cell phenotype, and particular genetic and epigenetic alterations are linked to biologically and clinically distinct subsets of CRC.
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            Dependency of colorectal cancer on a TGF-β-driven program in stromal cells for metastasis initiation.

            Alexandre Calon, Elisa Espinet, Sergio Palomo-Ponce … (2012)
            A large proportion of colorectal cancers (CRCs) display mutational inactivation of the TGF-β pathway, yet, paradoxically, they are characterized by elevated TGF-β production. Here, we unveil a prometastatic program induced by TGF-β in the microenvironment that associates with a high risk of CRC relapse upon treatment. The activity of TGF-β on stromal cells increases the efficiency of organ colonization by CRC cells, whereas mice treated with a pharmacological inhibitor of TGFBR1 are resilient to metastasis formation. Secretion of IL11 by TGF-β-stimulated cancer-associated fibroblasts (CAFs) triggers GP130/STAT3 signaling in tumor cells. This crosstalk confers a survival advantage to metastatic cells. The dependency on the TGF-β stromal program for metastasis initiation could be exploited to improve the diagnosis and treatment of CRC. Copyright © 2012 Elsevier Inc. All rights reserved.
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              Matrix stiffness drives Epithelial-Mesenchymal Transition and tumour metastasis through a TWIST1-G3BP2 mechanotransduction pathway

              Spencer Wei, Laurent Fattet, Jeff H. Tsai … (2015)
              Matrix stiffness potently regulates cellular behavior in various biological contexts. In breast tumours, the presence of dense clusters of collagen fibrils indicates increased matrix stiffness and correlates with poor survival. It is unclear how mechanical inputs are transduced into transcriptional outputs to drive tumour progression. Here we report that TWIST1 is an essential mechano-mediator that promotes epithelial-mesenchymal transition (EMT) in response to increasing matrix stiffness. High matrix stiffness promotes nuclear translocation of TWIST1 by releasing TWIST1 from its cytoplasmic binding partner G3BP2. Loss of G3BP2 leads to constitutive TWIST1 nuclear localization and synergizes with increasing matrix stiffness to induce EMT and promote tumour invasion and metastasis. In human breast tumours, collagen fiber alignment, a marker of increasing matrix stiffness, and reduced expression of G3BP2 together predict poor survival. Our findings reveal a TWIST1-G3BP2 mechanotransduction pathway that responds to biomechanical signals from the tumour microenvironment to drive EMT, invasion, and metastasis.
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                Author and article information

                Contributors
                Josep Baulida: jbaulida@imim.es
                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): 13 June 2017
                Publication date (Print): July 2017
                Volume: 11
                Issue: 7 , Special Issue: Epithelial‐to‐Mesenchymal Transition in Cancer ( doiID: 10.1002/mol2.2017.11.issue-7 )
                Pages: 847-859
                Affiliations
                [ 1 ] Programa de Recerca en CàncerInstitut Hospital del Mar d'Investigacions Mèdiques BarcelonaSpain
                Author notes
                [*] [* ] Correspondence

                J. Baulida, C/ Dr. Aiguader, 88. 08003, Barcelona, Spain

                Fax: +34 3 3160410

                Tel: +34 3 3160436

                E‐mail: jbaulida@ 123456imim.es

                Article
                Publisher ID: MOL212080
                DOI: 10.1002/1878-0261.12080
                PMC ID: 5496490
                PubMed ID: 28544627
                SO-VID: 6ae3cf9f-0a7f-4baa-82b8-b795a1bed424
                Copyright © © 2017 The Authors. Published by FEBS Press and John Wiley & Sons Ltd.
                License:

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

                History
                Date received : 17 February 2017
                Date revision received : 16 May 2017
                Date accepted : 18 May 2017
                Page count
                Figures: 2, Tables: 1, Pages: 13, Words: 8348
                Funding
                Funded by: Generalitat de Catalunya
                Award ID: 2014SGR32
                Funded by: Fundació IMIM
                Funded by: Fondo de Investigaciones Sanitarias of the Instituto Carlos III (ISCIII)/FEDER
                Award ID: PI15/00447
                Categories
                Subject: Review
                Subject: Reviews
                Custom metadata
                source-schema-version-number 2.0
                component-id mol212080
                cover-date July 2017
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_NLMPMC version:5.1.2 mode:remove_FC converted:04.07.2017

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: cancer‐associated fibroblasts,epithelial‐to‐mesenchymal transition transcription factors,snail,tumour–stroma crosstalk,twist,zeb
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: cancer‐associated fibroblasts, epithelial‐to‐mesenchymal transition transcription factors, snail, tumour–stroma crosstalk, twist, zeb

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