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Current Reviews in Clinical and Experimental Pharmacology

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Review Article

The Warburg Effect on Cancer Cells Survival: The Role of Sugar Starvation in Cancer Therapy

Author(s): Wissam Zam*, Imtissal Ahmed and Haneen Yousef

Volume 16, Issue 1, 2021

Published on: 13 April, 2020

Page: [30 - 38] Pages: 9

DOI: 10.2174/1574884715666200413121756

Abstract

Background: Cancer is not just one disease; it is a group of diseases either genetic or metabolic due to the malfunction of mitochondria. Thus, metabolic pathways are reprogrammed to satisfy tumor cell proliferation and survival requirements.

Methods: We undertook a structured search of bibliographic databases for peer-reviewed research literature dealing with these metabolic pathways.

Results: It was found that cancer cells prefer fermentation as a source of energy even in the presence of oxygen, this altered metabolism of cancer cells may confer a selective advantage for survival and proliferation according to the Warburg effect. Furthermore, some molecules like HIF, PKM2, NADPH and others are essential to the survival of cancer cells in the hypoxic abnormal environment which has limited glucose sources.

Conclusion: As cancer cells use glucose for aerobic glycolysis as a preferred substrate for energyyielding metabolism, we discuss in this review the Warburg effect and a strategy of starving cancer cells from glucose to prevent cancer cell survival and induce apoptosis in various types of cancer which could be the key to future treatment.

Keywords: Aerobic glycolysis, cancer cells, glucose starvation, hypoxic environment, warburg effect, apoptosis.

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[1]
Seyfried TN, Shelton LM. Cancer as a metabolic disease. Nutr Metab (Lond) 2010; 7(7): 7.
[http://dx.doi.org/10.1186/1743-7075-7-7] [PMID: 20181022]
[2]
Cairns RA, Harris IS, Mak TW. Regulation of cancer cell metabolism. Nat Rev Cancer 2011; 11(2): 85-95.
[http://dx.doi.org/10.1038/nrc2981] [PMID: 21258394]
[3]
Liou GY, Storz P. Reactive oxygen species in cancer. Free Radic Res 2010; 44(5): 479-96.
[http://dx.doi.org/10.3109/10715761003667554] [PMID: 20370557]
[4]
Oleksyszyn J, Wietrzyk J, Psurski M. Cancer could it be cured? A spontaneous regression of cancer, cancer energy metabolism, hyperglycemia-hypoglycemia, metformin, warburg and crabtree effects and a new perspective in cancer treatment. J Cancer Sci Ther 2014; 6(3): 56-61.
[5]
Reczek CR, Chandel NS. ROS promotes cancer cell survival through calcium signaling. Cancer Cell 2018; 33(6): 949-51.
[http://dx.doi.org/10.1016/j.ccell.2018.05.010] [PMID: 29894695]
[6]
Brewer TF, Garcia FJ, Onak CS, Carroll KS, Chang CJ. Chemical approaches to discovery and study of sources and targets of hydrogen peroxide redox signaling through NADPH oxidase proteins. Annu Rev Biochem 2015; 84: 765-90.
[http://dx.doi.org/10.1146/annurev-biochem-060614-034018] [PMID: 26034893]
[7]
Kumari S, Badana AK. G MM, G S, Malla R. Reactive oxygen species: A key constituent in cancer survival. Biomark Insights 2018; 131177271918755391
[http://dx.doi.org/10.1177/1177271918755391] [PMID: 29449774]
[8]
Felty Q, Singh KP, Roy D. Estrogen-induced G1/S transition of G0-arrested estrogen-dependent breast cancer cells is regulated by mitochondrial oxidant signaling. Oncogene 2005; 24(31): 4883-93.
[http://dx.doi.org/10.1038/sj.onc.1208667] [PMID: 15897899]
[9]
Ramsey MR, Sharpless NE. ROS as a tumour suppressor? Nat Cell Biol 2006; 8(11): 1213-5.
[http://dx.doi.org/10.1038/ncb1106-1213] [PMID: 17077852]
[10]
Han D, Antunes F, Canali R, Rettori D, Cadenas E. Voltage-dependent anion channels control the release of the superoxide anion from mitochondria to cytosol. J Biol Chem 2003; 278(8): 5557-63.
[http://dx.doi.org/10.1074/jbc.M210269200] [PMID: 12482755]
[11]
Fruehauf JP, Meyskens FL Jr. Reactive oxygen species: A breath of life or death? Clin Cancer Res 2007; 13(3): 789-94.
[http://dx.doi.org/10.1158/1078-0432.CCR-06-2082] [PMID: 17289868]
[12]
Schafer ZT, Grassian AR, Song L, et al. Antioxidant and oncogene rescue of metabolic defects caused by loss of matrix attachment. Nature 2009; 461(7260): 109-13.
[http://dx.doi.org/10.1038/nature08268] [PMID: 19693011]
[13]
Gorrini C, Harris IS, Mak TW. Modulation of oxidative stress as an anticancer strategy. Nat Rev Drug Discov 2013; 12(12): 931-47.
[http://dx.doi.org/10.1038/nrd4002] [PMID: 24287781]
[14]
Takahashi N, Chen HY, Harris IS, et al. Cancer cells co-opt the neuronal redox-sensing channel TRPA1 to promote oxidative stress tolerance. Cancer Cell 2018; 33(6): 985-1003.
[http://dx.doi.org/10.1016/j.ccell.2018.05.001] [PMID: 29805077]
[15]
Xu RH, Pelicano H, Zhou Y, et al. Inhibition of glycolysis in cancer cells: A novel strategy to overcome drug resistance associated with mitochondrial respiratory defect and hypoxia. Cancer Res 2005; 65(2): 613-21.
[PMID: 15695406]
[16]
Verrax J, Taper H, Buc Calderon P. Targeting cancer cells by an oxidant-based therapy. Curr Mol Pharmacol 2008; 1(1): 80-92.
[http://dx.doi.org/10.2174/1874467210801010080] [PMID: 20021426]
[17]
Warburg O. On the origin of cancer cells. Science 1956; 123(3191): 309-14.
[http://dx.doi.org/10.1126/science.123.3191.309] [PMID: 13298683]
[18]
Aykin-Burns N, Ahmad IM, Zhu Y, Oberley LW, Spitz DR. Increased levels of superoxide and H2O2 mediate the differential susceptibility of cancer cells versus normal cells to glucose deprivation. Biochem J 2009; 418(1): 29-37.
[http://dx.doi.org/10.1042/BJ20081258] [PMID: 18937644]
[19]
Boros LG, Lee PW, Brandes JL, et al. Nonoxidative pentose phosphate pathways and their direct role in ribose synthesis in tumors: is cancer a disease of cellular glucose metabolism? Med Hypotheses 1998; 50(1): 55-9.
[http://dx.doi.org/10.1016/S0306-9877(98)90178-5] [PMID: 9488183]
[20]
Buettner GR. Superoxide dismutase in redox biology: the roles of superoxide and hydrogen peroxide. Anticancer Agents Med Chem 2011; 11(4): 341-6.
[http://dx.doi.org/10.2174/187152011795677544] [PMID: 21453242]
[21]
Nogueira V, Hay N. Molecular pathways: Reactive oxygen species homeostasis in cancer cells and implications for cancer therapy. Clin Cancer Res 2013; 19(16): 4309-14.
[http://dx.doi.org/10.1158/1078-0432.CCR-12-1424] [PMID: 23719265]
[22]
Epstein T, Gatenby RA, Brown JS. The Warburg effect as an adaptation of cancer cells to rapid fluctuations in energy demand. PLoS One 2017; 12(9)e0185085
[http://dx.doi.org/10.1371/journal.pone.0185085] [PMID: 28922380]
[23]
Liberti MV, Locasale JW. The warburg effect: How does it benefit cancer cells? Trends Biochem Sci 2016; 41(3): 211-8.
[http://dx.doi.org/10.1016/j.tibs.2015.12.001] [PMID: 26778478]
[24]
Hanahan D, Weinberg RA. Hallmarks of cancer: The next generation. Cell 2011; 144(5): 646-74.
[http://dx.doi.org/10.1016/j.cell.2011.02.013] [PMID: 21376230]
[25]
Warburg O. The metabolism of carcinoma cells. J Cancer Res 1925; 9(1): 148-63.
[http://dx.doi.org/10.1158/jcr.1925.148]
[26]
Warburg O, Posener K, Negelein E. Ueber den stoffwechsel der tumoren. Biochem Z 1924; 152(1): 319-44.
[27]
Chang CH, Qiu J, O’Sullivan D, et al. Metabolic competition in the tumor microenvironment is a driver of cancer progression. Cell 2015; 162(6): 1229-41.
[http://dx.doi.org/10.1016/j.cell.2015.08.016] [PMID: 26321679]
[28]
Ho PC, Bihuniak JD, Macintyre AN, et al. Phosphoenolpyruvate Is a metabolic checkpoint of anti-tumor T cell responses. Cell 2015; 162(6): 1217-28.
[http://dx.doi.org/10.1016/j.cell.2015.08.012] [PMID: 26321681]
[29]
Pfeiffer T, Schuster S, Bonhoeffer S. Cooperation and competition in the evolution of ATP-producing pathways. Science 2001; 292(5516): 504-7.
[http://dx.doi.org/10.1126/science.1058079] [PMID: 11283355]
[30]
Slavov N, Budnik BA, Schwab D, Airoldi EM, van Oudenaarden A. Constant growth rate can be supported by decreasing energy flux and increasing aerobic glycolysis. Cell Rep 2014; 7(3): 705-14.
[http://dx.doi.org/10.1016/j.celrep.2014.03.057] [PMID: 24767987]
[31]
Gambhir SS. Molecular imaging of cancer with positron emission tomography. Nat Rev Cancer 2002; 2(9): 683-93.
[http://dx.doi.org/10.1038/nrc882] [PMID: 12209157]
[32]
Al Tameemi W, Dale TP, Al-Jumaily RMK, Forsyth NR. Hypoxia-Modified cancer cell metabolism. Front Cell Dev Biol 2019; 7: 4.
[http://dx.doi.org/10.3389/fcell.2019.00004] [PMID: 30761299]
[33]
Muri J, Heer S, Matsushita M, et al. The thioredoxin-1 system is essential for fueling DNA synthesis during T-cell metabolic reprogramming and proliferation. Nat Commun 2018; 9(1): 1851.
[http://dx.doi.org/10.1038/s41467-018-04274-w] [PMID: 29749372]
[34]
Vander Heiden MG, Cantley LC, Thompson CB. Understanding the Warburg effect: The metabolic requirements of cell proliferation. Science 2009; 324(5930): 1029-33.
[http://dx.doi.org/10.1126/science.1160809] [PMID: 19460998]
[35]
Epstein T, Xu L, Gillies RJ, Gatenby RA. Separation of metabolic supply and demand: Aerobic glycolysis as a normal physiological response to fluctuating energetic demands in the membrane. Cancer Metab 2014; 2: 7.
[http://dx.doi.org/10.1186/2049-3002-2-7] [PMID: 24982758]
[36]
Locasale JW, Cantley LC. Metabolic flux and the regulation of mammalian cell growth. Cell Metab 2011; 14(4): 443-51.
[http://dx.doi.org/10.1016/j.cmet.2011.07.014] [PMID: 21982705]
[37]
Lunt SY, Vander Heiden MG. Aerobic glycolysis: Meeting the metabolic requirements of cell proliferation. Annu Rev Cell Dev Biol 2011; 27: 441-64.
[http://dx.doi.org/10.1146/annurev-cellbio-092910-154237] [PMID: 21985671]
[38]
Bartrons R, Caro J. Hypoxia, glucose metabolism and the Warburg’s effect. J Bioenerg Biomembr 2007; 39(3): 223-9.
[http://dx.doi.org/10.1007/s10863-007-9080-3] [PMID: 17661163]
[39]
Weljie AM, Jirik FR. Hypoxia-induced metabolic shifts in cancer cells: moving beyond the Warburg effect. Int J Biochem Cell Biol 2011; 43(7): 981-9.
[http://dx.doi.org/10.1016/j.biocel.2010.08.009] [PMID: 20797448]
[40]
Kaelin WG Jr, Ratcliffe PJ. Oxygen sensing by metazoans: The central role of the HIF hydroxylase pathway. Mol Cell 2008; 30(4): 393-402.
[http://dx.doi.org/10.1016/j.molcel.2008.04.009] [PMID: 18498744]
[41]
Kaelin WG Jr, Thompson CBQ Q. &A: Cancer: Clues from cell metabolismNature 2010; 465(7298): 562-4.
[http://dx.doi.org/10.1038/465562a] [PMID: 20520704]
[42]
Mathupala SP, Rempel A, Pedersen PL. Glucose catabolism in cancer cells: identification and characterization of a marked activation response of the type II hexokinase gene to hypoxic conditions. J Biol Chem 2001; 276(46): 43407-12.
[http://dx.doi.org/10.1074/jbc.M108181200] [PMID: 11557773]
[43]
Semenza GL, Roth PH, Fang HM, Wang GL. Transcriptional regulation of genes encoding glycolytic enzymes by hypoxia-inducible factor 1. J Biol Chem 1994; 269(38): 23757-63.
[PMID: 8089148]
[44]
Gordan JD, Thompson CB, Simon MC. HIF and c-Myc: Sibling rivals for control of cancer cell metabolism and proliferation. Cancer Cell 2007; 12(2): 108-13.
[http://dx.doi.org/10.1016/j.ccr.2007.07.006] [PMID: 17692803]
[45]
Gleadle JM, Ratcliffe PJ. Induction of hypoxia-inducible factor-1, erythropoietin, vascular endothelial growth factor, and glucose transporter-1 by hypoxia: Evidence against a regulatory role for Src kinase. Blood 1997; 89(2): 503-9.
[http://dx.doi.org/10.1182/blood.V89.2.503] [PMID: 9002952]
[46]
Metallo CM, Gameiro PA, Bell EL, et al. Reductive glutamine metabolism by IDH1 mediates lipogenesis under hypoxia. Nature 2011; 481(7381): 380-4.
[http://dx.doi.org/10.1038/nature10602] [PMID: 22101433]
[47]
Mullen AR, Wheaton WW, Jin ES, et al. Reductive carboxylation supports growth in tumour cells with defective mitochondria. Nature 2011; 481(7381): 385-8.
[http://dx.doi.org/10.1038/nature10642] [PMID: 22101431]
[48]
Hsu PP, Sabatini DM. Cancer cell metabolism: Warburg and beyond. Cell 2008; 134(5): 703-7.
[http://dx.doi.org/10.1016/j.cell.2008.08.021] [PMID: 18775299]
[49]
Moreno-Sánchez R, Marín-Hernández A, Saavedra E, Pardo JP, Ralph SJ, Rodríguez-Enríquez S. Who controls the ATP supply in cancer cells? Biochemistry lessons to understand cancer energy metabolism. Int J Biochem Cell Biol 2014; 50: 10-23.
[http://dx.doi.org/10.1016/j.biocel.2014.01.025] [PMID: 24513530]
[50]
Dong G, Mao Q, Xia W, et al. PKM2 and cancer: The function of PKM2 beyond glycolysis. Oncol Lett 2016; 11(3): 1980-6.
[http://dx.doi.org/10.3892/ol.2016.4168] [PMID: 26998110]
[51]
Christofk HR, Vander Heiden MG, Harris MH, et al. The M2 splice isoform of pyruvate kinase is important for cancer metabolism and tumour growth. Nature 2008; 452(7184): 230-3.
[http://dx.doi.org/10.1038/nature06734] [PMID: 18337823]
[52]
Ferguson EC, Rathmell JC. New roles for pyruvate kinase M2: Working out the Warburg effect. Trends Biochem Sci 2008; 33(8): 359-62.
[http://dx.doi.org/10.1016/j.tibs.2008.05.006] [PMID: 18603432]
[53]
Chen L, Zhang Z, Hoshino A, et al. NADPH production by the oxidative pentose-phosphate pathway supports folate metabolism. Nat Metab 2019; 1: 404-15.
[http://dx.doi.org/10.1038/s42255-019-0043-x] [PMID: 31058257]
[54]
Moreira JD, Hamraz M, Abolhassani M, et al. The redox status of cancer cells supports mechanisms behind the warburg effect. Metabolites 2016; 6(4): 33.
[http://dx.doi.org/10.3390/metabo6040033] [PMID: 27706102]
[55]
Diaz-Moralli S, Tarrado-Castellarnau M, Miranda A, Cascante M. Targeting cell cycle regulation in cancer therapy. Pharmacol Ther 2013; 138(2): 255-71.
[http://dx.doi.org/10.1016/j.pharmthera.2013.01.011] [PMID: 23356980]
[56]
Gatenby RA, Gillies RJ. Why do cancers have high aerobic glycolysis? Nat Rev Cancer 2004; 4(11): 891-9.
[http://dx.doi.org/10.1038/nrc1478] [PMID: 15516961]
[57]
Fabregat I, Vitorica J, Satrustegui J, Machado A. The pentose phosphate cycle is regulated by NADPH/NADP ratio in rat liver. Arch Biochem Biophys 1985; 236(1): 110-8.
[http://dx.doi.org/10.1016/0003-9861(85)90610-1] [PMID: 3966788]
[58]
Yu FX, Dai RP, Goh SR, Zheng L, Luo Y. Logic of a mammalian metabolic cycle: An oscillated NAD+/NADH redox signaling regulates coordinated histone expression and S-phase progression. Cell Cycle 2009; 8(5): 773-9.
[http://dx.doi.org/10.4161/cc.8.5.7880] [PMID: 19221488]
[59]
Fabregat I, Revilla E, Machado A. Short-term control of the pentose phosphate cycle by insulin could be modulated by the NADPH/NADP ratio in rat adipocytes and hepatocytes. Biochem Biophys Res Commun 1987; 146(2): 920-5.
[http://dx.doi.org/10.1016/0006-291X(87)90618-8] [PMID: 3304289]
[60]
DeBerardinis RJ, Lum JJ, Hatzivassiliou G, Thompson CB. The biology of cancer: Metabolic reprogramming fuels cell growth and proliferation. Cell Metab 2008; 7(1): 11-20.
[http://dx.doi.org/10.1016/j.cmet.2007.10.002] [PMID: 18177721]
[61]
Kapelner A, Vorsanger M. Starvation of cancer via induced ketogenesis and severe hypoglycemia. Med Hypotheses 2015; 84(3): 162-8.
[http://dx.doi.org/10.1016/j.mehy.2014.11.002] [PMID: 25579853]
[62]
Baracca A, Chiaradonna F, Sgarbi G, Solaini G, Alberghina L, Lenaz G. Mitochondrial Complex I decrease is responsible for bioenergetic dysfunction in K-ras transformed cells. Biochim Biophys Acta 2010; 1797(2): 314-23.
[http://dx.doi.org/10.1016/j.bbabio.2009.11.006] [PMID: 19931505]
[63]
Palorini R, De Rasmo D, Gaviraghi M, et al. Oncogenic K-ras expression is associated with derangement of the cAMP/PKA pathway and forskolin-reversible alterations of mitochondrial dynamics and respiration. Oncogene 2013; 32(3): 352-62.
[http://dx.doi.org/10.1038/onc.2012.50] [PMID: 22410778]
[64]
Caro-Maldonado A, Tait SW, Ramírez-Peinado S, et al. Glucose deprivation induces an atypical form of apoptosis mediated by caspase-8 in Bax-, Bak-deficient cells. Cell Death Differ 2010; 17(8): 1335-44.
[http://dx.doi.org/10.1038/cdd.2010.21] [PMID: 20203689]
[65]
Yuneva M, Zamboni N, Oefner P, Sachidanandam R, Lazebnik Y. Deficiency in glutamine but not glucose induces MYC-dependent apoptosis in human cells. J Cell Biol 2007; 178(1): 93-105.
[http://dx.doi.org/10.1083/jcb.200703099] [PMID: 17606868]
[66]
Galaris D, Pantopoulos K. Oxidative stress and iron homeostasis: mechanistic and health aspects. Crit Rev Clin Lab Sci 2008; 45(1): 1-23.
[http://dx.doi.org/10.1080/10408360701713104] [PMID: 18293179]
[67]
Circu ML, Aw TY. Reactive oxygen species, cellular redox systems, and apoptosis. Free Radic Biol Med 2010; 48(6): 749-62.
[http://dx.doi.org/10.1016/j.freeradbiomed.2009.12.022] [PMID: 20045723]
[68]
Dang CV. Links between metabolism and cancer. Genes Dev 2012; 26(9): 877-90.
[http://dx.doi.org/10.1101/gad.189365.112] [PMID: 22549953]
[69]
Palorini R, Cammarata FP, Balestrieri C, et al. Glucose starvation induces cell death in K-ras-transformed cells by interfering with the hexosamine biosynthesis pathway and activating the unfolded protein response. Cell Death Dis 2013; 4e732..
[http://dx.doi.org/10.1038/cddis.2013.257] [PMID: 23868065]
[70]
Bassik MC, Scorrano L, Oakes SA, Pozzan T, Korsmeyer SJ. Phosphorylation of BCL-2 regulates ER Ca2+ homeostasis and apoptosis. EMBO J 2004; 23(5): 1207-16.
[http://dx.doi.org/10.1038/sj.emboj.7600104] [PMID: 15010700]
[71]
Wei Y, Sinha S, Levine B. Dual role of JNK1-mediated phosphorylation of Bcl-2 in autophagy and apoptosis regulation. Autophagy 2008; 4(7): 949-51.
[http://dx.doi.org/10.4161/auto.6788] [PMID: 18769111]
[72]
Ron D, Walter P. Signal integration in the endoplasmic reticulum unfolded protein response. Nat Rev Mol Cell Biol 2007; 8(7): 519-29.
[http://dx.doi.org/10.1038/nrm2199] [PMID: 17565364]
[73]
Rutkowski DT, Kaufman RJ. That which does not kill me makes me stronger: Adapting to chronic ER stress. Trends Biochem Sci 2007; 32(10): 469-76.
[http://dx.doi.org/10.1016/j.tibs.2007.09.003] [PMID: 17920280]
[74]
Gonzalez-Menendez P, Hevia D, Alonso-Arias R, et al. GLUT1 protects prostate cancer cells from glucose deprivation-induced oxidative stress. Redox Biol 2018; 17: 112-27.
[http://dx.doi.org/10.1016/j.redox.2018.03.017] [PMID: 29684818]
[75]
Kim HS, Kim MJ, Lim J, Yang Y, Lee MS, Lim JS. NDRG2 overexpression enhances glucose deprivation-mediated apoptosis in breast cancer cells via inhibition of the LKB1-AMPK pathway. Genes Cancer 2014; 5(5-6): 175-85.
[PMID: 25061501]
[76]
Sato K, Tsuchihara K, Fujii S, et al. Autophagy is activated in colorectal cancer cells and contributes to the tolerance to nutrient deprivation. Cancer Res 2007; 67(20): 9677-84.
[http://dx.doi.org/10.1158/0008-5472.CAN-07-1462] [PMID: 17942897]
[77]
Lee HY, Itahana Y, Schuechner S, et al. Ca2+-dependent demethylation of phosphatase PP2Ac promotes glucose deprivation-induced cell death independently of inhibiting glycolysis. Sci Signal 2018; 11(512): 7893.
[http://dx.doi.org/10.1126/scisignal.aam7893] [PMID: 29317521]
[78]
Di Conza G, Trusso Cafarello S, Zheng X, Zhang Q, Mazzone M. PHD2 targeting overcomes breast cancer cell death upon glucose starvation in a PP2A/B55α-mediated manner. Cell Rep 2017; 18(12): 2836-44.
[http://dx.doi.org/10.1016/j.celrep.2017.02.081] [PMID: 28329677]
[79]
Roberts HR, Smartt HJM, Greenhough A, Moore AE, Williams AC, Paraskeva C. Colon tumour cells increase PGE(2) by regulating COX-2 and 15-PGDH to promote survival during the microenvironmental stress of glucose deprivation. Carcinogenesis 2011; 32(11): 1741-7.
[http://dx.doi.org/10.1093/carcin/bgr210] [PMID: 21926111]
[80]
Zhang M, Liu T, Sun H, et al. Pim1 supports human colorectal cancer growth during glucose deprivation by enhancing the Warburg effect. Cancer Sci 2018; 109(5): 1468-79.
[http://dx.doi.org/10.1111/cas.13562] [PMID: 29516572]
[81]
Graham NA, Tahmasian M, Kohli B, et al. Glucose deprivation activates a metabolic and signaling amplification loop leading to cell death. Mol Syst Biol 2012; 8(589): 589.
[http://dx.doi.org/10.1038/msb.2012.20] [PMID: 22735335]
[82]
Buzzai M, Bauer DE, Jones RG, et al. The glucose dependence of Akt-transformed cells can be reversed by pharmacologic activation of fatty acid beta-oxidation. Oncogene 2005; 24(26): 4165-73.
[http://dx.doi.org/10.1038/sj.onc.1208622] [PMID: 15806154]
[83]
Mathews EH, Stander BA, Joubert AM, Liebenberg L. Tumor cell culture survival following glucose and glutamine deprivation at typical physiological concentrations. Nutrition 2014; 30(2): 218-27.
[http://dx.doi.org/10.1016/j.nut.2013.07.024] [PMID: 24262514]
[84]
Li Y, Liu L, Tollefsbol TO. Glucose restriction can extend normal cell lifespan and impair precancerous cell growth through epigenetic control of hTERT and p16 expression. FASEB J 2010; 24(5): 1442-53.
[http://dx.doi.org/10.1096/fj.09-149328] [PMID: 20019239]
[85]
Priebe A, Tan L, Wahl H, et al. Glucose deprivation activates AMPK and induces cell death through modulation of Akt in ovarian cancer cells. Gynecol Oncol 2011; 122(2): 389-95.
[http://dx.doi.org/10.1016/j.ygyno.2011.04.024] [PMID: 21570709]
[86]
Kueck A, Opipari AW Jr, Griffith KA, et al. Resveratrol inhibits glucose metabolism in human ovarian cancer cells. Gynecol Oncol 2007; 107(3): 450-7.
[http://dx.doi.org/10.1016/j.ygyno.2007.07.065] [PMID: 17825886]
[87]
Wang S, Mao Y, Xi S, Wang X, Sun L. Nutrient starvation sensitizes human ovarian cancer SKOV3 cells to BH3 mimetic via modulation of mitochondrial dynamics. Anat Rec (Hoboken) 2017; 300(2): 326-39.
[http://dx.doi.org/10.1002/ar.23454] [PMID: 27486855]
[88]
Kanska J, Aspuria PP, Taylor-Harding B, et al. Glucose deprivation elicits phenotypic plasticity via ZEB1-mediated expression of NNMT. Oncotarget 2017; 8(16): 26200-20.
[http://dx.doi.org/10.18632/oncotarget.15429] [PMID: 28412735]
[89]
Leithner K, Hrzenjak A, Trötzmüller M, et al. PCK2 activation mediates an adaptive response to glucose depletion in lung cancer. Oncogene 2015; 34(8): 1044-50.
[http://dx.doi.org/10.1038/onc.2014.47] [PMID: 24632615]
[90]
He N, Kim N, Jeong E, Lu Y, Mills GB, Yoon S. Glucose starvation induces mutation and lineage-dependent adaptive responses in a large collection of cancer cell lines. Int J Oncol 2016; 48(1): 67-72.
[http://dx.doi.org/10.3892/ijo.2015.3242] [PMID: 26573869]
[91]
Shim H, Chun YS, Lewis BC, Dang CV. A unique glucose-dependent apoptotic pathway induced by c-Myc. Proc Natl Acad Sci USA 1998; 95(4): 1511-6.
[http://dx.doi.org/10.1073/pnas.95.4.1511] [PMID: 9465046]
[92]
Vincent EE, Sergushichev A, Griss T, et al. Mitochondrial phosphoenolpyruvate carboxykinase regulates metabolic adaptation and enables glucose-independent tumor growth. Mol Cell 2015; 60(2): 195-207.
[http://dx.doi.org/10.1016/j.molcel.2015.08.013] [PMID: 26474064]
[93]
Bowker SL, Majumdar SR, Veugelers P, Johnson JA. Increased cancer-related mortality for patients with type 2 diabetes who use sulfonylureas or insulin: Response to Farooki and Schneider. Diabetes Care 2006; 29(8): 1990-1.
[http://dx.doi.org/10.2337/dc06-0997] [PMID: 16873829]
[94]
Shaw RJ, Lamia KA, Vasquez D, et al. The kinase LKB1 mediates glucose homeostasis in liver and therapeutic effects of metformin. Science 2005; 310(5754): 1642-6.
[http://dx.doi.org/10.1126/science.1120781] [PMID: 16308421]
[95]
Bikas A, Jensen K, Patel A, et al. Glucose-deprivation increases thyroid cancer cells sensitivity to metformin. Endocr Relat Cancer 2015; 22(6): 919-32.
[http://dx.doi.org/10.1530/ERC-15-0402] [PMID: 26362676]
[96]
Biswal BN, Das SN, Das BK, Rath R. Alteration of cellular metabolism in cancer cells and its therapeutic prospects. J Oral Maxillofac Pathol 2017; 21(2): 244-51.
[http://dx.doi.org/10.4103/jomfp.JOMFP_60_17] [PMID: 28932034]
[97]
Le QT, Chen E, Salim A, et al. An evaluation of tumor oxygenation and gene expression in patients with early stage non-small cell lung cancers. Clin Cancer Res 2006; 12(5): 1507-14.
[http://dx.doi.org/10.1158/1078-0432.CCR-05-2049] [PMID: 16533775]
[98]
Galvez AS, Duran A, Linares JF, et al. Protein kinase Czeta represses the interleukin-6 promoter and impairs tumorigenesis in vivo. Mol Cell Biol 2009; 29(1): 104-15.
[http://dx.doi.org/10.1128/MCB.01294-08] [PMID: 18955501]
[99]
Fang S, Fang X. Advances in glucose metabolism research in colorectal cancer. Biomed Rep 2016; 5(3): 289-95.
[http://dx.doi.org/10.3892/br.2016.719] [PMID: 27602209]
[100]
Ma L, Tao Y, Duran A, et al. Control of nutrient stress-induced metabolic reprogramming by PKCζ in tumorigenesis. Cell 2013; 152(3): 599-611.
[http://dx.doi.org/10.1016/j.cell.2012.12.028] [PMID: 23374352]
[101]
Iansante V, Choy PM, Fung SW, et al. PARP14 promotes the Warburg effect in hepatocellular carcinoma by inhibiting JNK1-dependent PKM2 phosphorylation and activationNat Commun 2015; 6: 7882.
[http://dx.doi.org/10.1038/ncomms8882] [PMID: 26258887]

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