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      The fuel and engine: The roles of reprogrammed metabolism in metastasis of primary liver cancer

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          Abstract

          Metastasis and metabolism reprogramming are two major hallmarks of cancer. In the initiation and progression of cancer, tumor cells are known to undergo fundamental metabolic changes to sustain their development and progression. In recent years, much more attentions have been drawn to their important roles in facilitating cancer metastasis through regulating the biological properties. In this review, we summarized the recent progresses in the studies of metabolism reprogramming of cancer metastasis, particularly of primary liver cancer, and highlight their potential applications.

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          Pyruvate kinase M2 is a PHD3-stimulated coactivator for hypoxia-inducible factor 1.

          Weibo Luo, Hongxia Hu, Ryan Chang … (2011)
          The pyruvate kinase isoforms PKM1 and PKM2 are alternatively spliced products of the PKM2 gene. PKM2, but not PKM1, alters glucose metabolism in cancer cells and contributes to tumorigenesis by mechanisms that are not explained by its known biochemical activity. We show that PKM2 gene transcription is activated by hypoxia-inducible factor 1 (HIF-1). PKM2 interacts directly with the HIF-1α subunit and promotes transactivation of HIF-1 target genes by enhancing HIF-1 binding and p300 recruitment to hypoxia response elements, whereas PKM1 fails to regulate HIF-1 activity. Interaction of PKM2 with prolyl hydroxylase 3 (PHD3) enhances PKM2 binding to HIF-1α and PKM2 coactivator function. Mass spectrometry and anti-hydroxyproline antibody assays demonstrate PKM2 hydroxylation on proline-403/408. PHD3 knockdown inhibits PKM2 coactivator function, reduces glucose uptake and lactate production, and increases O(2) consumption in cancer cells. Thus, PKM2 participates in a positive feedback loop that promotes HIF-1 transactivation and reprograms glucose metabolism in cancer cells. Copyright © 2011 Elsevier Inc. All rights reserved.
          Article 0 comments Cited 516 times – based on 0 reviews     Review now
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            Immunological hallmarks of stromal cells in the tumour microenvironment.

            Shannon Turley, Viviana Cremasco, Jillian L. Astarita (2015)
            A dynamic and mutualistic interaction between tumour cells and the surrounding stroma promotes the initiation, progression, metastasis and chemoresistance of solid tumours. Far less understood is the relationship between the stroma and tumour-infiltrating leukocytes; however, emerging evidence suggests that the stromal compartment can shape antitumour immunity and responsiveness to immunotherapy. Thus, there is growing interest in elucidating the immunomodulatory roles of the stroma that evolve within the tumour microenvironment. In this Review, we discuss the evidence that stromal determinants interact with leukocytes and influence antitumour immunity, with emphasis on the immunological attributes of stromal cells that may foster their protumorigenic function.
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              The glucose transporter Glut1 is selectively essential for CD4 T cell activation and effector function.

              Andrew N. Macintyre, Valerie Gerriets, Amanda G Nichols … (2014)
              CD4 T cell activation leads to proliferation and differentiation into effector (Teff) or regulatory (Treg) cells that mediate or control immunity. While each subset prefers distinct glycolytic or oxidative metabolic programs in vitro, requirements and mechanisms that control T cell glucose uptake and metabolism in vivo are uncertain. Despite expression of multiple glucose transporters, Glut1 deficiency selectively impaired metabolism and function of thymocytes and Teff. Resting T cells were normal until activated, when Glut1 deficiency prevented increased glucose uptake and glycolysis, growth, proliferation, and decreased Teff survival and differentiation. Importantly, Glut1 deficiency decreased Teff expansion and the ability to induce inflammatory disease in vivo. Treg cells, in contrast, were enriched in vivo and appeared functionally unaffected and able to suppress Teff, irrespective of Glut1 expression. These data show a selective in vivo requirement for Glut1 in metabolic reprogramming of CD4 T cell activation and Teff expansion and survival. Copyright © 2014 Elsevier Inc. All rights reserved.
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                Author and article information

                Contributors
                Lun-Xiu Qin
                Journal
                Journal ID (nlm-ta): Genes Dis
                Journal ID (iso-abbrev): Genes Dis
                Title: Genes & Diseases
                Publisher: Chongqing Medical University
                ISSN (Print): 2352-4820
                ISSN (Electronic): 2352-3042
                Publication date PMC-release: 07 February 2020
                Publication date Collection: September 2020
                Publication date (Electronic): 07 February 2020
                Volume: 7
                Issue: 3
                Pages: 299-307
                Affiliations
                [1]Department of General Surgery, Huashan Hospital, Cancer Metastasis Institute, Fudan University, 12 Urumqi Road (M), Shanghai, 200040, China
                Author notes
                [∗ ]Corresponding author. qinlx@ 123456fudan.edu.cn
                [1]

                Equal contributors.

                Article
                Publisher ID: S2352-3042(20)30024-6
                DOI: 10.1016/j.gendis.2020.01.016
                PMC ID: 7452537
                SO-VID: 872da93b-b789-41c2-8493-d5360168eae6
                Copyright statement: © 2020 Chongqing Medical University. Production and hosting by Elsevier B.V.
                License:

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

                History
                Date received : 22 October 2019
                Date revision received : 30 December 2019
                Date accepted : 28 January 2020
                Categories
                Subject: Article

                Keywords: amino acid,cancer metastasis,cholesterol,fatty acid,glucose,primary liver cancer,tumor microenvironment
                Data availability:
                Keywords: amino acid, cancer metastasis, cholesterol, fatty acid, glucose, primary liver cancer, tumor microenvironment

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