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      Role of tumor and host autophagy in cancer metabolism

      review-article
      1 , 1 , 2
      Genes & Development
      Cold Spring Harbor Laboratory Press
      autophagy, cancer, metabolism

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          Abstract

          In this review, Poillet-Perez et al. discuss how understanding the underlying mechanisms by which autophagy functions in cancer can guide its development as an anticancer approach.

          Abstract

          Macroautophagy (referred to here as autophagy) degrades and recycles cytoplasmic constituents to sustain cellular and mammalian metabolism and survival during starvation. Deregulation of autophagy is involved in numerous diseases, such as cancer. Cancers up-regulate autophagy and depend on it for survival, growth, and malignancy in a tumor cell-autonomous fashion. Recently, it has become apparent that autophagy in host tissues as well as the tumor cells themselves contribute to tumor growth. Understanding how autophagy regulates metabolism and tumor growth has revealed new essential tumor nutrients, where they come from, and how they are supplied and used, which can now be targeted for cancer therapy.

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          Most cited references107

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          The Emerging Hallmarks of Cancer Metabolism.

          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.
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            Fundamentals of cancer metabolism

            Researchers provide a conceptual framework to understand current knowledge of the fundamentals of cancer metabolism.
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              Autophagy fights disease through cellular self-digestion.

              Autophagy, or cellular self-digestion, is a cellular pathway involved in protein and organelle degradation, with an astonishing number of connections to human disease and physiology. For example, autophagic dysfunction is associated with cancer, neurodegeneration, microbial infection and ageing. Paradoxically, although autophagy is primarily a protective process for the cell, it can also play a role in cell death. Understanding autophagy may ultimately allow scientists and clinicians to harness this process for the purpose of improving human health.
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                Author and article information

                Journal
                Genes Dev
                Genes Dev
                genesdev
                genesdev
                GAD
                Genes & Development
                Cold Spring Harbor Laboratory Press
                0890-9369
                1549-5477
                1 June 2019
                : 33
                : 11-12
                : 610-619
                Affiliations
                [1 ]Rutgers Cancer Institute of New Jersey, New Brunswick, New Jersey 08903, USA;
                [2 ]Department of Molecular Biology and Biochemistry, Rutgers University, Piscataway, New Jersey 08854, USA
                Author notes
                Corresponding author: epwhite@ 123456cinj.rutgers.edu
                Article
                8711660
                10.1101/gad.325514.119
                6546058
                31160394
                0c8d5fe6-4df1-4edb-b027-b5cccc538532
                © 2019 Poillet-Perez and White; Published by Cold Spring Harbor Laboratory Press

                This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

                History
                Page count
                Pages: 10
                Funding
                Funded by: National Institutes of Health , open-funder-registry 10.13039/100000002;
                Award ID: R01CA163591
                Funded by: New Jersey Commission for Cancer Research
                Award ID: DHFS16PPC034
                Categories
                7
                4
                Review

                autophagy,cancer,metabolism
                autophagy, cancer, metabolism

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