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      2-Deoxy-d-Glucose and Its Analogs: From Diagnostic to Therapeutic Agents

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          Abstract

          The ability of 2-deoxy- d-glucose (2-DG) to interfere with d-glucose metabolism demonstrates that nutrient and energy deprivation is an efficient tool to suppress cancer cell growth and survival. Acting as a d-glucose mimic, 2-DG inhibits glycolysis due to formation and intracellular accumulation of 2-deoxy- d-glucose-6-phosphate (2-DG6P), inhibiting the function of hexokinase and glucose-6-phosphate isomerase, and inducing cell death. In addition to glycolysis inhibition, other molecular processes are also affected by 2-DG. Attempts to improve 2-DG’s drug-like properties, its role as a potential adjuvant for other chemotherapeutics, and novel 2-DG analogs as promising new anticancer agents are discussed in this review.

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          Mitochondrial autophagy is an HIF-1-dependent adaptive metabolic response to hypoxia.

          Huafeng Zhang, Marta Bosch-Marce, Larissa Shimoda … (2008)
          Autophagy is a process by which cytoplasmic organelles can be catabolized either to remove defective structures or as a means of providing macromolecules for energy generation under conditions of nutrient starvation. In this study we demonstrate that mitochondrial autophagy is induced by hypoxia, that this process requires the hypoxia-dependent factor-1-dependent expression of BNIP3 and the constitutive expression of Beclin-1 and Atg5, and that in cells subjected to prolonged hypoxia, mitochondrial autophagy is an adaptive metabolic response which is necessary to prevent increased levels of reactive oxygen species and cell death.
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            ER stress: Autophagy induction, inhibition and selection.

            Harun or Rashid, Raj Yadav, Hyung-Ryong Kim … (2015)
            An accumulation of unfolded or misfolded proteins in the endoplasmic reticulum (ER) leads to stress conditions. To mitigate such circumstances, stressed cells activate a homeostatic intracellular signaling network cumulatively called the unfolded protein response (UPR), which orchestrates the recuperation of ER function. Macroautophagy (hereafter autophagy), an intracellular lysosome-mediated bulk degradation pathway for recycling and eliminating wornout proteins, protein aggregates, and damaged organelles, has also emerged as an essential protective mechanism during ER stress. These 2 systems are dynamically interconnected, and recent investigations have revealed that ER stress can either stimulate or inhibit autophagy. However, the stress-associated molecular cues that control the changeover switch between induction and inhibition of autophagy are largely obscure. This review summarizes the crosstalk between ER stress and autophagy and their signaling networks mainly in mammalian-based systems. Additionally, we highlight current knowledge on selective autophagy and its connection to ER stress.
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              The coordinate regulation of the p53 and mTOR pathways in cells.

              Zhaohui Feng, Haiyan Zhang, Arnold J. Levine … (2005)
              Cell growth and proliferation requires an intricate coordination between the stimulatory signals arising from nutrients and growth factors and the inhibitory signals arising from intracellular and extracellular stresses. Alteration of the coordination often causes cancer. In mammals, the mTOR (mammalian target of rapamycin) protein kinase is the central node in nutrient and growth factor signaling, and p53 plays a critical role in sensing genotoxic and other stresses. The results presented here demonstrate that activation of p53 inhibits mTOR activity and regulates its downstream targets, including autophagy, a tumor suppression process. Moreover, the mechanisms by which p53 regulates mTOR involves AMP kinase activation and requires the tuberous sclerosis (TSC) 1/TSC2 complex, both of which respond to energy deprivation in cells. In addition, glucose starvation not only signals to shut down mTOR, but also results in the transient phosphorylation of the p53 protein. Thus, p53 and mTOR signaling machineries can cross-talk and coordinately regulate cell growth, proliferation, and death.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Mol Sci
                Journal ID (iso-abbrev): Int J Mol Sci
                Journal ID (publisher-id): ijms
                Title: International Journal of Molecular Sciences
                Publisher: MDPI
                ISSN (Electronic): 1422-0067
                Publication date (Electronic): 29 December 2019
                Publication date Collection: January 2020
                Volume: 21
                Issue: 1
                Electronic Location Identifier: 234
                Affiliations
                [1 ]Independent Laboratory of Genetic and Molecular Biology, Kaczkowski Military Institute of Hygiene and Epidemiology, Kozielska 4, 01-163 Warsaw, Poland; ewelinasiwiak1@ 123456op.pl (E.S.); maja.soltyka@ 123456gmail.com (M.S.); ancpatrin@ 123456gmail.com (A.J.); radoslaw.borowski@ 123456wpdpharmaceuticals.com (R.B.); domoradzki.tomasz@ 123456gmail.com (T.D.)
                [2 ]Texas Oncology, Division of Gynecologic Oncology, 910 E. Houston Street, Tyler, TX 75702, USA; aanyy@ 123456mac.com
                [3 ]Department of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, 1901 East Rd., Houston, TX 77054, USA; rziel77@ 123456gmail.com (R.Z.); ifokt@ 123456mdanderson.org (I.F.)
                [4 ]Biological and Chemical Research Centre, Department of Chemistry, University of Warsaw, 02-089 Warsaw, Poland; mziemniak@ 123456chem.uw.edu.pl
                Author notes
                [* ]Correspondence: bepaj@ 123456wp.pl (B.P.); wpriebe@ 123456mac.com (W.P.)
                [†]

                These authors contributed equally to this work.

                Author information
                https://orcid.org/0000-0002-3565-8860
                https://orcid.org/0000-0003-1454-0852
                Article
                Publisher ID: ijms-21-00234
                DOI: 10.3390/ijms21010234
                PMC ID: 6982256
                PubMed ID: 31905745
                SO-VID: a4f08922-0850-49ed-8bf2-f8b9b5c474f9
                Copyright © © 2019 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 22 November 2019
                Date accepted : 26 December 2019
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular biology
                Keywords: 2-deoxy-d-glucose,2-dg analogs,glioblastoma,anticancer therapy
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: 2-deoxy-d-glucose, 2-dg analogs, glioblastoma, anticancer therapy

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