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      Viral hijacking of cellular metabolism

      review-article
      Author(s): 1 , 2 , 1 , 3 , 4 ,
      Publication date (Electronic):
      Journal: BMC Biology
      Publisher: BioMed Central

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          Abstract

          This review discusses the current state of the viral metabolism field and gaps in knowledge that will be important for future studies to investigate. We discuss metabolic rewiring caused by viruses, the influence of oncogenic viruses on host cell metabolism, and the use of viruses as guides to identify critical metabolic nodes for cancer anabolism. We also discuss the need for more mechanistic studies identifying viral proteins responsible for metabolic hijacking and for in vivo studies of viral-induced metabolic rewiring. Improved technologies for detailed metabolic measurements and genetic manipulation will lead to important discoveries over the next decade.

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          Most cited references152

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          The Emerging Hallmarks of Cancer Metabolism.

          Natalya Pavlova, Craig B Thompson (2016)
          Tumorigenesis is dependent on the reprogramming of cellular metabolism as both direct and indirect consequence of oncogenic mutations. A common feature of cancer cell metabolism is the ability to acquire necessary nutrients from a frequently nutrient-poor environment and utilize these nutrients to both maintain viability and build new biomass. The alterations in intracellular and extracellular metabolites that can accompany cancer-associated metabolic reprogramming have profound effects on gene expression, cellular differentiation, and the tumor microenvironment. In this Perspective, we have organized known cancer-associated metabolic changes into six hallmarks: (1) deregulated uptake of glucose and amino acids, (2) use of opportunistic modes of nutrient acquisition, (3) use of glycolysis/TCA cycle intermediates for biosynthesis and NADPH production, (4) increased demand for nitrogen, (5) alterations in metabolite-driven gene regulation, and (6) metabolic interactions with the microenvironment. While few tumors display all six hallmarks, most display several. The specific hallmarks exhibited by an individual tumor may ultimately contribute to better tumor classification and aid in directing treatment.
          Article 0 comments Cited 1525 times – based on 0 reviews     Review now
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            Targeting HIF-1 for cancer therapy.

            Gregg L. Semenza (2003)
            Hypoxia-inducible factor 1 (HIF-1) activates the transcription of genes that are involved in crucial aspects of cancer biology, including angiogenesis, cell survival, glucose metabolism and invasion. Intratumoral hypoxia and genetic alterations can lead to HIF-1alpha overexpression, which has been associated with increased patient mortality in several cancer types. In preclinical studies, inhibition of HIF-1 activity has marked effects on tumour growth. Efforts are underway to identify inhibitors of HIF-1 and to test their efficacy as anticancer therapeutics.
            Article 0 comments Cited 634 times – based on 0 reviews     Review now
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              Hepatocellular carcinoma: epidemiology and molecular carcinogenesis.

              Hashem El-Serag, K Rudolph (2007)
              Primary liver cancer, which consists predominantly of hepatocellular carcinoma (HCC), is the fifth most common cancer worldwide and the third most common cause of cancer mortality. HCC has several interesting epidemiologic features including dynamic temporal trends; marked variations among geographic regions, racial and ethnic groups, and between men and women; and the presence of several well-documented environmental potentially preventable risk factors. Moreover, there is a growing understanding on the molecular mechanisms inducing hepatocarcinogenesis, which almost never occurs in healthy liver, but the cancer risk increases sharply in response to chronic liver injury at the cirrhosis stage. A detailed understanding of epidemiologic factors and molecular mechanisms associated with HCC ultimately could improve our current concepts for screening and treatment of this disease.
              Article 0 comments Cited 520 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Heather R. Christofk: hchristofk@mednet.ucla.edu
                Journal
                Journal ID (nlm-ta): BMC Biol
                Journal ID (iso-abbrev): BMC Biol
                Title: BMC Biology
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1741-7007
                Publication date (Electronic): 18 July 2019
                Publication date PMC-release: 18 July 2019
                Publication date Collection: 2019
                Volume: 17
                Electronic Location Identifier: 59
                Affiliations
                [1 ]ISNI 0000 0000 9632 6718, GRID grid.19006.3e, Department of Biological Chemistry, David Geffen School of Medicine, , University of California, Los Angeles (UCLA), ; Los Angeles, CA 90095 USA
                [2 ]ISNI 0000 0000 9632 6718, GRID grid.19006.3e, Department of Pediatrics, Division of Hematology/Oncology, , David Geffen School of Medicine, UCLA, ; Los Angeles, CA 90095 USA
                [3 ]ISNI 0000 0000 9632 6718, GRID grid.19006.3e, Jonsson Comprehensive Cancer Center, UCLA, ; Los Angeles, CA 90095 USA
                [4 ]ISNI 0000 0000 9632 6718, GRID grid.19006.3e, Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, UCLA, ; Los Angeles, CA 90095 USA
                Article
                Publisher ID: 678
                DOI: 10.1186/s12915-019-0678-9
                PMC ID: 6637495
                PubMed ID: 31319842
                SO-VID: 940d3fe4-9362-4af7-97b5-a7e3dc336644
                Copyright © © The Author(s). 2019
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/100000048, American Cancer Society;
                Award ID: RSG-16-111-01-MPC
                Funded by: FundRef http://dx.doi.org/10.13039/100000002, National Institutes of Health;
                Award ID: CA215185-01
                Award ID: GM008042
                Award Recipient :
                Funded by: Jonsson Comprehensive Cancer Center (US)
                Award ID: Jonsson Comprehensive Cancer Center (US)
                Funded by: FundRef http://dx.doi.org/10.13039/100007185, University of California, Los Angeles;
                Award ID: T32AI060567
                Award ID: T32 CA009056
                Award Recipient :
                Funded by: University of California, Los Angeles (US)
                Award ID: T32 CA009056
                Award Recipient :
                Categories
                Subject: Review
                Custom metadata
                issue-copyright-statement © The Author(s) 2019

                ScienceOpen disciplines: Life sciences
                Data availability:
                ScienceOpen disciplines: Life sciences

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