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      TGFΒ-induced transcription in cancer

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          Abstract

          The Transforming Growth Factor-beta (TGFβ) pathway mediates a broad spectrum of cellular processes and is involved in several diseases, including cancer. TGFβ has a dual role in tumours, acting as a tumour suppressor in the early phase of tumorigenesis and as a tumour promoter in more advanced stages. In this review, we discuss the effects of TGFβ-driven transcription on all stages of tumour progression, with special focus on lung cancer. Since some TGFβ target genes are specifically involved in promoting metastasis, we speculate that these genes might be good targets to block tumour progression without compromising the tumour suppressor effects of the TGFβ pathway.

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          Microenvironmental regulation of metastasis.

          Johanna A. Joyce, Jeffrey W Pollard (2009)
          Metastasis is a multistage process that requires cancer cells to escape from the primary tumour, survive in the circulation, seed at distant sites and grow. Each of these processes involves rate-limiting steps that are influenced by non-malignant cells of the tumour microenvironment. Many of these cells are derived from the bone marrow, particularly the myeloid lineage, and are recruited by cancer cells to enhance their survival, growth, invasion and dissemination. This Review describes experimental data demonstrating the role of the microenvironment in metastasis, identifies areas for future research and suggests possible new therapeutic avenues.
          Article 0 comments Cited 1196 times – based on 0 reviews     Review now
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            TGFbeta in the context of an inflammatory cytokine milieu supports de novo differentiation of IL-17-producing T cells.

            Marc Veldhoen, Richard J Hocking, Christopher Atkins … (2006)
            We describe de novo generation of IL-17-producing T cells from naive CD4 T cells, induced in cocultures of naive CD4 T cells and naturally occurring CD4+ CD25+ T cells (Treg) in the presence of TLR3, TLR4, or TLR9 stimuli. Treg can be substituted by TGFbeta1, which, together with the proinflammatory cytokine IL-6, supports the differentiation of IL-17-producing T cells, a process that is amplified by IL-1beta and TNFalpha. We could not detect a role for IL-23 in the differentiation of IL-17-producing T cells but confirmed its importance for their survival and expansion. Transcription factors GATA-3 and T-bet, as well as its target Hlx, are absent in IL-17-producing T cells, and they do not express the negative regulator for TGFbeta signaling, Smad7. Our data indicate that, in the presence of IL-6, TGFbeta1 subverts Th1 and Th2 differentiation for the generation of IL-17-producing T cells.
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              Metastasis: a question of life or death.

              Patrick Mehlen, Alain Puisieux (2006)
              The metastatic process is highly inefficient--very few of the many cells that migrate from the primary tumour successfully colonize distant sites. One proposed mechanism to explain this inefficiency is provided by the cancer stem cell model, which hypothesizes that micrometastases can only be established by tumour stem cells, which are few in number. However, recent in vitro and in vivo observations indicate that apoptosis is an important process regulating metastasis. Here we stress that the inhibition of cell death, apart from its extensively described function in primary tumour development, is a crucial characteristic of metastatic cancer cells.
              Article 0 comments Cited 595 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Victoria Sanz-Moreno
                Journal
                Journal ID (nlm-ta): Semin Cancer Biol
                Journal ID (iso-abbrev): Semin. Cancer Biol
                Title: Seminars in Cancer Biology
                Publisher: Academic Press
                ISSN (Print): 1044-579X
                ISSN (Electronic): 1096-3650
                Publication date PMC-release: 1 February 2017
                Publication date (Print): February 2017
                Volume: 42
                Pages: 60-69
                Affiliations
                [0005]Tumour Plasticity Laboratory, Randall Division of Cell and Molecular Biophysics, New Hunt’s House, Guy’s Campus, King’s College London, London SE1 1UL, UK
                Author notes
                [* ]Corresponding author. victoria.sanz_moreno@ 123456kcl.ac.uk
                [1]

                These authors contributed equally to this work.

                Article
                Publisher ID: S1044-579X(16)30042-6
                DOI: 10.1016/j.semcancer.2016.08.009
                PMC ID: 6137079
                PubMed ID: 27586372
                SO-VID: 8f7dba7e-3978-48a0-9452-0b1e7f7c4dd9
                Copyright © © 2016 Elsevier Ltd. All rights reserved.
                License:

                This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 17 June 2016
                Date accepted : 19 August 2016
                Categories
                Subject: Article

                Keywords: tgfβ,cancer,metastasis,transcription,emt,immunosurveillance
                Data availability:
                Keywords: tgfβ, cancer, metastasis, transcription, emt, immunosurveillance

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