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      • Record: found
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      Is Open Access

      SOCS, inflammation, and cancer

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          Abstract

          Signal transduction pathways elicited by cytokines and hormones have been shown to regulate distinct stages of development. Suppressor of cytokine signaling (SOCS) proteins are negative feedback regulators of cytokine signaling mediated by the JAK-STAT signaling pathway. In particular, SOCS1 and SOCS3 are potent inhibitors of JAKs and can play pivotal roles in inflammation, as well as in the development and progression of cancers. Abnormal expression of SOCS1 and SOCS3 in cancer cells has been reported in human carcinoma associated with dysregulation of signals from cytokine receptors, Toll-like receptors (TLRs), and hormone receptors, resulting in malignancies. In this review, we focus on the role of SOCS1 and SOCS3 in cancer development. In addition, the potential of SOCS as a therapeutic target and diagnostic aid will be discussed.

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          Lessons from hereditary colorectal cancer.

          K Kinzler, B Vogelstein (1996)
          Article 0 comments Cited 426 times – based on 0 reviews     Review now
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            The weight of leptin in immunity.

            Antonio La Cava, Giuseppe Matarese (2004)
            Leptin is an adipocyte-derived hormone/cytokine that links nutritional status with neuroendocrine and immune functions. As a hormone, leptin regulates food intake and basal metabolism, and is sexually dimorphic - that is, its serum concentration is higher in females than in males with a similar body fat mass. As a cytokine, leptin can affect thymic homeostasis and the secretion of acute-phase reactants such as interleukin-1 and tumour-necrosis factor. Similar to other pro-inflammatory cytokines, leptin promotes T helper 1 (TH1)-cell differentiation and can modulate the onset and progression of autoimmune responses in several animal models of disease. Here, we review the advances and controversy for a role of leptin in the pathophysiology of immune responses.
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              Targeting Stat3 blocks both HIF-1 and VEGF expression induced by multiple oncogenic growth signaling pathways.

              Qing Qing Xu, Jon J Briggs, Sungman Park … (2005)
              Vascular endothelial growth factor (VEGF) upregulation is induced by many receptor and intracellular oncogenic proteins commonly activated in cancer, rendering molecular targeting of VEGF expression a complex challenge. While VEGF inducers abound, only two major transcription activators have been identified for its promoter: hypoxia inducible factor-1 (HIF-1) and signal transducer and activator of transcription (Stat3). Both HIF-1 expression and Stat3 activity are upregulated in diverse cancers. Here, we provide evidence that Stat3 is required for both basal and growth signal-induced expression of HIF-1. Moreover, induction of VEGF by diverse oncogenic growth stimuli, including IL-6R, c-Src, Her2/Neu, is attenuated in cells without Stat3 signaling. We further demonstrate that Stat3 regulates expression of Akt, which is required for growth signal-induced HIF-1 upregulation. Targeting Stat3 with a small-molecule inhibitor blocks HIF-1 and VEGF expression in vitro and inhibits tumor growth and angiogenesis in vivo. Furthermore, tumor cells' in vivo angiogenic capacity induced by IL-6R, which simultaneously activates Jak/STAT and PI3K/Akt pathways, is abrogated when Stat3 is inhibited. Activation of Stat3 signaling by various growth signaling is prevalent in diverse cancers. Results presented here demonstrate that Stat3 is an effective target for inhibiting tumor VEGF expression and angiogenesis.
              Article 0 comments Cited 187 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): JAKSTAT
                Journal ID (iso-abbrev): JAKSTAT
                Journal ID (publisher-id): JKST
                Title: JAK-STAT
                Publisher: Landes Bioscience
                ISSN (Print): 2162-3988
                ISSN (Electronic): 2162-3996
                Publication date (Print): 01 July 2013
                Publication date (Electronic): 15 August 2013
                Publication date PMC-release: 15 August 2013
                Volume: 2
                Issue: 3
                Electronic Location Identifier: e24053
                Affiliations
                [1 ]Department of Gastroenterology; Research Center for Hepatitis and Immunology; Research Institute; National Center for Global Health and Medicine (NCGM); Ichikawa, Japan
                [2 ]Department of Microbiology and Immunology; Keio University School of Medicine; Tokyo, Japan
                [3 ]Japan Science and Technology Agency (JST); CREST; Tokyo, Japan
                Author notes
                [* ]Correspondence to: Akihiko Yoshimura; Email: yoshimura@ 123456a6.keio.jp
                Article
                Publisher ID: 2013JAKS0132R Publisher Item ID: 24053
                DOI: 10.4161/jkst.24053
                PMC ID: 3772102
                PubMed ID: 24069550
                SO-VID: 219d4540-f8be-47f5-9f77-6271eefa2333
                Copyright © Copyright © 2013 Landes Bioscience
                License:

                This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.

                History
                Date received : 21 January 2013
                Date revision received : 20 February 2013
                Date accepted : 20 February 2013
                Categories
                Subject: Review

                Keywords: socs,stat,cancer,inflammation,therapeutic target
                Data availability:
                Keywords: socs, stat, cancer, inflammation, therapeutic target

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