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Published in: Tumor Biology 4/2015

01-04-2015 | Research Article

Targeting prostate cancer cell metabolism: impact of hexokinase and CPT-1 enzymes

Authors: Rouhallah Najjar Sadeghi, Fatemeh Karami-Tehrani, Siamak Salami

Published in: Tumor Biology | Issue 4/2015

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Abstract

Glycolysis has been shown to be required for the cell growth and proliferation in several cancer cells. However, prostate cancer cells were accused of using more fatty acid than glucose to meet their bioenergetic demands. The present study was designed to evaluate the involvement of hexokinase and CPT-1 in the cell growth and proliferation of human prostate cancer cell lines, PC3, and LNCaP-FGC-10. Hexokinase and CPT-1 activities were examined in the presence of different concentrations of their inhibitors, lonidamine and etomoxir, to find the concentration of maximum inhibition ([I max]). To assess cell viability and proliferation, dimethylthiazol (MTT) assay was carried out using [I max] for 24, 48, and 72 h on PC3 and LNCaP cells. Apoptosis was determined using annexin-V, caspase-3 activity assay, Hoechst 33258 staining, and evaluation of mitochondrial membrane potential (MMP). Moreover, ATP levels were measured following lonidamine and etomoxir exposure. In addition, to define the impact of exogenous fatty acid on the cell growth and proliferation, CPT-1 activity was evaluated in the presence of palmitate (50 μM). Hexokinase and CPT-1 activities were significantly inhibited by lonidamine [600 μM] and etomoxir [100 μM] in both cell lines. Treatment of the cells with lonidamine [600 μM] resulted in a significant ATP reduction, cell viability and apoptosis, caspase-3 activity elevation, MMP reduction, and appearance of apoptosis-related morphological changes in the cells. In contrast, etomoxir [100 μM] just decreased ATP levels in both cell lines without significant cell death and apoptosis. Compared with glucose (2 g/L), palmitate intensified CPT-1 activity in both cell lines, especially in LNCaP cells. In addition, activity of CPT-1 was higher in LNCaP than PC3 cells. Our results suggest that prostate cancer cells may metabolize glucose as a source of bioenergetic pathways. ATP could also be produced by long-chain fatty acid oxidation. In addition, these data might suggest that LNCaP is more compatible with palmitate.
Literature
1.
go back to reference Warburg O. Über den stoffwechsel menschlicher tumorzellen. J Mol Med. 1925;4:2396–7. Warburg O. Über den stoffwechsel menschlicher tumorzellen. J Mol Med. 1925;4:2396–7.
2.
go back to reference Pouysségur J, Dayan F, Mazure NM. Hypoxia signalling in cancer and approaches to enforce tumour regression. Nature. 2006;441:437–43.CrossRefPubMed Pouysségur J, Dayan F, Mazure NM. Hypoxia signalling in cancer and approaches to enforce tumour regression. Nature. 2006;441:437–43.CrossRefPubMed
3.
go back to reference Koukourakis MI, Giatromanolaki A, Harris AL, Sivridis E. Comparison of metabolic pathways between cancer cells and stromal cells in colorectal carcinomas: a metabolic survival role for tumor-associated stroma. Cancer Res. 2006;66:632–7.CrossRefPubMed Koukourakis MI, Giatromanolaki A, Harris AL, Sivridis E. Comparison of metabolic pathways between cancer cells and stromal cells in colorectal carcinomas: a metabolic survival role for tumor-associated stroma. Cancer Res. 2006;66:632–7.CrossRefPubMed
4.
go back to reference Swietach P, Vaughan-Jones RD, Harris AL. Regulation of tumor pH and the role of carbonic anhydrase 9. Cancer Metastasis Rev. 2007;26:299–310.CrossRefPubMed Swietach P, Vaughan-Jones RD, Harris AL. Regulation of tumor pH and the role of carbonic anhydrase 9. Cancer Metastasis Rev. 2007;26:299–310.CrossRefPubMed
5.
go back to reference Gatenby RA, Gillies RJ. Why do cancers have high aerobic glycolysis? Nat Rev Cancer. 2004;4:891–9.CrossRefPubMed Gatenby RA, Gillies RJ. Why do cancers have high aerobic glycolysis? Nat Rev Cancer. 2004;4:891–9.CrossRefPubMed
6.
go back to reference Ben Sahra I, Laurent K, Giuliano S, Larbret F, Ponzio G, Gounon P, et al. Targeting cancer cell metabolism: the combination of metformin and 2-deoxyglucose induces p53-dependent apoptosis in prostate cancer cells. Cancer Res. 2010;70:2465–75.CrossRefPubMed Ben Sahra I, Laurent K, Giuliano S, Larbret F, Ponzio G, Gounon P, et al. Targeting cancer cell metabolism: the combination of metformin and 2-deoxyglucose induces p53-dependent apoptosis in prostate cancer cells. Cancer Res. 2010;70:2465–75.CrossRefPubMed
7.
go back to reference Wood TE, Dalili S, Simpson CD, Hurren R, Mao X, Saiz FS, et al. A novel inhibitor of glucose uptake sensitizes cells to FAS-induced cell death. Mol Cancer Ther. 2008;7:3546–55.CrossRefPubMed Wood TE, Dalili S, Simpson CD, Hurren R, Mao X, Saiz FS, et al. A novel inhibitor of glucose uptake sensitizes cells to FAS-induced cell death. Mol Cancer Ther. 2008;7:3546–55.CrossRefPubMed
8.
go back to reference Singh G, Lakkis CL, Laucirica R, Epner DE. Regulation of prostate cancer cell division by glucose. J Cell Physiol. 1999;180:431–8.CrossRefPubMed Singh G, Lakkis CL, Laucirica R, Epner DE. Regulation of prostate cancer cell division by glucose. J Cell Physiol. 1999;180:431–8.CrossRefPubMed
9.
go back to reference Liu Y. Fatty acid oxidation is a dominant bioenergetic pathway in prostate cancer. Prostate Cancer Prostatic Dis. 2006;9:230–4.CrossRefPubMed Liu Y. Fatty acid oxidation is a dominant bioenergetic pathway in prostate cancer. Prostate Cancer Prostatic Dis. 2006;9:230–4.CrossRefPubMed
10.
go back to reference Liu Y, Zuckier LS, Ghesani NV. Dominant uptake of fatty acid over glucose by prostate cells: a potential new diagnostic and therapeutic approach. Anticancer Res. 2010;30:369–74.PubMed Liu Y, Zuckier LS, Ghesani NV. Dominant uptake of fatty acid over glucose by prostate cells: a potential new diagnostic and therapeutic approach. Anticancer Res. 2010;30:369–74.PubMed
11.
go back to reference Sinha K. Elevated α-methylacyl-CoA racemase enzymatic activity. Am J Pathol2004;164:787-793 Sinha K. Elevated α-methylacyl-CoA racemase enzymatic activity. Am J Pathol2004;164:787-793
12.
go back to reference Rubin M, Zhou M, Dhanasekaran SM. α-Methylacyl-CoA racemase as tissue biomarker of PC. JAMA 2002;287:1662-1670 Rubin M, Zhou M, Dhanasekaran SM. α-Methylacyl-CoA racemase as tissue biomarker of PC. JAMA 2002;287:1662-1670
13.
go back to reference Luo J, Zha S, Gage WR, Dunn TA, et al. α-Methylacyl-CoA racemase; a new molecular marker for prostate cancer. Cancer Res 2002; 62:2220–2226. Luo J, Zha S, Gage WR, Dunn TA, et al. α-Methylacyl-CoA racemase; a new molecular marker for prostate cancer. Cancer Res 2002; 62:2220–2226.
14.
go back to reference Jiang Z, W.B.A., Rock K L, Xu Y, Savas L, Khan A, et al., P504S: a new molecular marker for the detection of prostate carcinoma. Am J Surg Pathol 2001; 25:13971404. Jiang Z, W.B.A., Rock K L, Xu Y, Savas L, Khan A, et al., P504S: a new molecular marker for the detection of prostate carcinoma. Am J Surg Pathol 2001; 25:13971404.
15.
go back to reference Zhou M, Chinnaiyan AM, Kleer CG, Lucas PC, Rubin MA. Alpha-methylacyl-CoA racemase: a novel tumor marker over-expressed in several human cancers and their precursor lesions. Am J Surg Pathol 2002; 26:926-931. Zhou M, Chinnaiyan AM, Kleer CG, Lucas PC, Rubin MA. Alpha-methylacyl-CoA racemase: a novel tumor marker over-expressed in several human cancers and their precursor lesions. Am J Surg Pathol 2002; 26:926-931.
16.
go back to reference Zha S, Ferdinandusse S, Hicks JL, Denis S, Dunn TA, Wanders RJ, et al. Peroxisomal branched chain fatty acid beta-oxidation pathway is upregulated in prostate cancer. Prostate. 2005;63:316–23.CrossRefPubMed Zha S, Ferdinandusse S, Hicks JL, Denis S, Dunn TA, Wanders RJ, et al. Peroxisomal branched chain fatty acid beta-oxidation pathway is upregulated in prostate cancer. Prostate. 2005;63:316–23.CrossRefPubMed
17.
go back to reference Brawer MK. Lonidamine: basic science and rationale for treatment of prostatic proliferative disorders. Rev Urol. 2005;7(7):S21–6.PubMedPubMedCentral Brawer MK. Lonidamine: basic science and rationale for treatment of prostatic proliferative disorders. Rev Urol. 2005;7(7):S21–6.PubMedPubMedCentral
18.
go back to reference Floridi A, Paggi MG, Marcante ML, Silvestrini B, Caputo A, de Martino C. Lonidamine, a selective inhibitor of aerobic glycolysis of murine tumor cells. J Natl Cancer Inst. 1981;66:497–9.PubMed Floridi A, Paggi MG, Marcante ML, Silvestrini B, Caputo A, de Martino C. Lonidamine, a selective inhibitor of aerobic glycolysis of murine tumor cells. J Natl Cancer Inst. 1981;66:497–9.PubMed
19.
go back to reference Floridi A, Paggi MG, D'Atri S, De Martino C, Marcante ML, Silvestrini B, et al. Effect of lonidamine on the energy metabolism of Ehrlich ascites tumor cells. Cancer Res. 1981;41:4661–6.PubMed Floridi A, Paggi MG, D'Atri S, De Martino C, Marcante ML, Silvestrini B, et al. Effect of lonidamine on the energy metabolism of Ehrlich ascites tumor cells. Cancer Res. 1981;41:4661–6.PubMed
20.
go back to reference Bustamante E, Pedersen PL. High aerobic glycolysis of rat hepatoma cells in culture: role of mitochondrial hexokinase. Proc Natl Acad Sci. 1977;74:3735–9.CrossRefPubMedPubMedCentral Bustamante E, Pedersen PL. High aerobic glycolysis of rat hepatoma cells in culture: role of mitochondrial hexokinase. Proc Natl Acad Sci. 1977;74:3735–9.CrossRefPubMedPubMedCentral
21.
go back to reference Xu FY, Taylor WA, Hurd JA, Hatch GM. Etomoxir mediates differential metabolic channeling of fatty acid and glycerol precursors into cardiolipin in H9c2 cells. J Lipid Res. 2003;44:415–23.CrossRefPubMed Xu FY, Taylor WA, Hurd JA, Hatch GM. Etomoxir mediates differential metabolic channeling of fatty acid and glycerol precursors into cardiolipin in H9c2 cells. J Lipid Res. 2003;44:415–23.CrossRefPubMed
22.
go back to reference Morillas M, Clotet J, Rubí B, Serra D, Arino J, Hegardt F, et al. Inhibition by etomoxir of rat liver carnitine octanoyltransferase is produced through the co-ordinate interaction with two histidine residues. Biochem J. 2000;351:495–502.CrossRefPubMedPubMedCentral Morillas M, Clotet J, Rubí B, Serra D, Arino J, Hegardt F, et al. Inhibition by etomoxir of rat liver carnitine octanoyltransferase is produced through the co-ordinate interaction with two histidine residues. Biochem J. 2000;351:495–502.CrossRefPubMedPubMedCentral
23.
go back to reference Gerondaes P, Alberti K, Agius L. Interactions of inhibitors of carnitine palmitoyltransferase I and fibrates in cultured hepatocytes. Biochem J. 1988;253:169–73.CrossRefPubMedPubMedCentral Gerondaes P, Alberti K, Agius L. Interactions of inhibitors of carnitine palmitoyltransferase I and fibrates in cultured hepatocytes. Biochem J. 1988;253:169–73.CrossRefPubMedPubMedCentral
24.
go back to reference Listenberger LL, Ory DS, Schaffer JE. Palmitate-induced apoptosis can occur through a ceramide-independent pathway. J Biol Chem. 2001;276:14890–5.CrossRefPubMed Listenberger LL, Ory DS, Schaffer JE. Palmitate-induced apoptosis can occur through a ceramide-independent pathway. J Biol Chem. 2001;276:14890–5.CrossRefPubMed
25.
go back to reference Robey RB, Raval BJ, Ma J, Santos AV. Thrombin is a novel regulator of hexokinase activity in mesangial cells. Kidney Int. 2000;57:2308–18.CrossRefPubMed Robey RB, Raval BJ, Ma J, Santos AV. Thrombin is a novel regulator of hexokinase activity in mesangial cells. Kidney Int. 2000;57:2308–18.CrossRefPubMed
26.
go back to reference Karlic H, Lohninger S, Koeck T, Lohninger A. Dietary l-carnitine stimulates carnitine acyltransferases in the liver of aged rats. J Histochem Cytochem. 2002;50:205–12.CrossRefPubMed Karlic H, Lohninger S, Koeck T, Lohninger A. Dietary l-carnitine stimulates carnitine acyltransferases in the liver of aged rats. J Histochem Cytochem. 2002;50:205–12.CrossRefPubMed
27.
go back to reference Salami S, Karami-Tehrani F. Biochemical studies of apoptosis induced by tamoxifen in estrogen receptor positive and negative breast cancer cell lines. Clin Biochem. 2003;36:247–53.CrossRefPubMed Salami S, Karami-Tehrani F. Biochemical studies of apoptosis induced by tamoxifen in estrogen receptor positive and negative breast cancer cell lines. Clin Biochem. 2003;36:247–53.CrossRefPubMed
28.
go back to reference Perry SW, Norman JP, Barbieri J, Brown EB, Gelbard HA. Mitochondrial membrane potential probes and the proton gradient: a practical usage guide. Biotechniques. 2011;50:98.CrossRefPubMedPubMedCentral Perry SW, Norman JP, Barbieri J, Brown EB, Gelbard HA. Mitochondrial membrane potential probes and the proton gradient: a practical usage guide. Biotechniques. 2011;50:98.CrossRefPubMedPubMedCentral
29.
go back to reference Srinivasan S, Stevens M, Wiley JW. Diabetic peripheral neuropathy: evidence for apoptosis and associated mitochondrial dysfunction. Diabetes. 2000;49:1932–8.CrossRefPubMed Srinivasan S, Stevens M, Wiley JW. Diabetic peripheral neuropathy: evidence for apoptosis and associated mitochondrial dysfunction. Diabetes. 2000;49:1932–8.CrossRefPubMed
30.
go back to reference Epstein JI, Carmichael M, Partin AW. OA-519 (fatty acid synthase) as an independent predictor of pathologic state in adenocarcinoma of the prostate. Urology. 1995;45:81–6.CrossRefPubMed Epstein JI, Carmichael M, Partin AW. OA-519 (fatty acid synthase) as an independent predictor of pathologic state in adenocarcinoma of the prostate. Urology. 1995;45:81–6.CrossRefPubMed
31.
go back to reference Rossi S, Graner E, Febbo P, Weinstein L, Bhattacharya N, Onody T, et al. Fatty acid synthase expression defines distinct molecular signatures in prostate cancer. Mol Cancer Res. 2003;1:707–15.PubMed Rossi S, Graner E, Febbo P, Weinstein L, Bhattacharya N, Onody T, et al. Fatty acid synthase expression defines distinct molecular signatures in prostate cancer. Mol Cancer Res. 2003;1:707–15.PubMed
32.
go back to reference Oudard S, Poirson F, Miccoli L, Bourgeois Y, Vassault A, Poisson M, et al. Mitochondria-bound hexokinase as target for therapy of malignant gliomas. Int J Cancer. 1995;62:216–22.CrossRefPubMed Oudard S, Poirson F, Miccoli L, Bourgeois Y, Vassault A, Poisson M, et al. Mitochondria-bound hexokinase as target for therapy of malignant gliomas. Int J Cancer. 1995;62:216–22.CrossRefPubMed
33.
go back to reference Wilson JE. Isozymes of mammalian hexokinase: structure, subcellular localization and metabolic function. J Exp Biol. 2003;206:2049–57.CrossRefPubMed Wilson JE. Isozymes of mammalian hexokinase: structure, subcellular localization and metabolic function. J Exp Biol. 2003;206:2049–57.CrossRefPubMed
34.
go back to reference Kumaravel G, Gandour R, Krueger M, Ramsay R. Comparison of the active sites of the purified carnitine acyltransferases from peroxisomes and mitochondria by using a reaction-intermediate analogue. Biochem J. 1993;294:645–51.CrossRefPubMedPubMedCentral Kumaravel G, Gandour R, Krueger M, Ramsay R. Comparison of the active sites of the purified carnitine acyltransferases from peroxisomes and mitochondria by using a reaction-intermediate analogue. Biochem J. 1993;294:645–51.CrossRefPubMedPubMedCentral
35.
go back to reference Murthy M, Pande SV. Malonyl-CoA binding site and the overt carnitine palmitoyltransferase activity reside on the opposite sides of the outer mitochondrial membrane. Proc Natl Acad Sci. 1987;84:378–82.CrossRefPubMedPubMedCentral Murthy M, Pande SV. Malonyl-CoA binding site and the overt carnitine palmitoyltransferase activity reside on the opposite sides of the outer mitochondrial membrane. Proc Natl Acad Sci. 1987;84:378–82.CrossRefPubMedPubMedCentral
36.
go back to reference Pimenta AS, Gaidhu MP, Habib S, So M, Fediuc S, Mirpourian M, et al. Prolonged exposure to palmitate impairs fatty acid oxidation despite activation of AMP-activated protein kinase in skeletal muscle cells. J Cell Physiol. 2008;217:478–85.CrossRefPubMed Pimenta AS, Gaidhu MP, Habib S, So M, Fediuc S, Mirpourian M, et al. Prolonged exposure to palmitate impairs fatty acid oxidation despite activation of AMP-activated protein kinase in skeletal muscle cells. J Cell Physiol. 2008;217:478–85.CrossRefPubMed
37.
go back to reference Nomura DK, Lombardi DP, Chang JW, Niessen S, Ward AM, Long JZ, et al. Monoacylglycerol lipase exerts dual control over endocannabinoid and fatty acid pathways to support prostate cancer. Chem Biol. 2011;18:846–56.CrossRefPubMedPubMedCentral Nomura DK, Lombardi DP, Chang JW, Niessen S, Ward AM, Long JZ, et al. Monoacylglycerol lipase exerts dual control over endocannabinoid and fatty acid pathways to support prostate cancer. Chem Biol. 2011;18:846–56.CrossRefPubMedPubMedCentral
38.
go back to reference Higgins L, Withers H, Garbens A, Love H, Magnoni L, Hayward S, et al. Hypoxia and the metabolic phenotype of prostate cancer cells. Biochim Biophys Acta (BBA)-Bioenerg. 2009;1787:1433–43.CrossRef Higgins L, Withers H, Garbens A, Love H, Magnoni L, Hayward S, et al. Hypoxia and the metabolic phenotype of prostate cancer cells. Biochim Biophys Acta (BBA)-Bioenerg. 2009;1787:1433–43.CrossRef
39.
go back to reference Zaugg K, Yao Y, Reilly PT, Kannan K, Kiarash R, Mason J, et al. Carnitine palmitoyltransferase 1C promotes cell survival and tumor growth under conditions of metabolic stress. Genes Dev. 2011;25:1041–51.CrossRefPubMedPubMedCentral Zaugg K, Yao Y, Reilly PT, Kannan K, Kiarash R, Mason J, et al. Carnitine palmitoyltransferase 1C promotes cell survival and tumor growth under conditions of metabolic stress. Genes Dev. 2011;25:1041–51.CrossRefPubMedPubMedCentral
40.
go back to reference Ruderman NB, Dean D. Malonyl CoA, long chain fatty acyl CoA and insulin resistance in skeletal muscle. J Basic Clin Physiol Pharmacol. 1998;9:295–308.CrossRefPubMed Ruderman NB, Dean D. Malonyl CoA, long chain fatty acyl CoA and insulin resistance in skeletal muscle. J Basic Clin Physiol Pharmacol. 1998;9:295–308.CrossRefPubMed
41.
go back to reference Pike LS, Smift AL, Croteau NJ, Ferrick DA, Wu M. Inhibition of fatty acid oxidation by etomoxir impairs NADPH production and increases reactive oxygen species resulting in ATP depletion and cell death in human glioblastoma cells. Biochim Biophys Acta (BBA)-Bioenerg. 2011;1807:726–34.CrossRef Pike LS, Smift AL, Croteau NJ, Ferrick DA, Wu M. Inhibition of fatty acid oxidation by etomoxir impairs NADPH production and increases reactive oxygen species resulting in ATP depletion and cell death in human glioblastoma cells. Biochim Biophys Acta (BBA)-Bioenerg. 2011;1807:726–34.CrossRef
42.
go back to reference Kim C, Wong J, Wen J, Wang S, Wang C, Spiering S, et al. Studying arrhythmogenic right ventricular dysplasia with patient-specific iPSCs. Nature. 2013;105–10. Kim C, Wong J, Wen J, Wang S, Wang C, Spiering S, et al. Studying arrhythmogenic right ventricular dysplasia with patient-specific iPSCs. Nature. 2013;105–10.
44.
go back to reference Pouyssegur J, Franchi A, Silvestre P. Relationship between increased aerobic glycolysis and DNA synthesis initiation studied using glycolytic mutant fibroblasts. Nature. 1980;287:445–7.CrossRefPubMed Pouyssegur J, Franchi A, Silvestre P. Relationship between increased aerobic glycolysis and DNA synthesis initiation studied using glycolytic mutant fibroblasts. Nature. 1980;287:445–7.CrossRefPubMed
45.
go back to reference Jannière L, Canceill D, Suski C, Kanga S, Dalmais B, Lestini R, et al. Genetic evidence for a link between glycolysis and DNA replication. PLoS One. 2007;2:e447.CrossRefPubMedPubMedCentral Jannière L, Canceill D, Suski C, Kanga S, Dalmais B, Lestini R, et al. Genetic evidence for a link between glycolysis and DNA replication. PLoS One. 2007;2:e447.CrossRefPubMedPubMedCentral
46.
go back to reference Farese RV, Standaert ML, Arnold TP, Yamada K, Musunuru K, Hernandez H, et al. Preferential activation of microsomal diacylglycerol/protein kinase C signaling during glucose treatment (de novo phospholipid synthesis) of rat adipocytes. J Clin Investig. 1994;93:1894–9.CrossRefPubMedPubMedCentral Farese RV, Standaert ML, Arnold TP, Yamada K, Musunuru K, Hernandez H, et al. Preferential activation of microsomal diacylglycerol/protein kinase C signaling during glucose treatment (de novo phospholipid synthesis) of rat adipocytes. J Clin Investig. 1994;93:1894–9.CrossRefPubMedPubMedCentral
47.
go back to reference Miele C, Paturzo F, Teperino R, Sakane F, Fiory F, Oriente F, et al. Glucose regulates diacylglycerol intracellular levels and protein kinase C activity by modulating diacylglycerol kinase subcellular localization. J Biol Chem. 2007;282:31835–43.CrossRefPubMed Miele C, Paturzo F, Teperino R, Sakane F, Fiory F, Oriente F, et al. Glucose regulates diacylglycerol intracellular levels and protein kinase C activity by modulating diacylglycerol kinase subcellular localization. J Biol Chem. 2007;282:31835–43.CrossRefPubMed
48.
go back to reference Burg JS, Espenshade PJ. Glucose controls phosphoregulation of HMG-CoA reductase through the PP2A-related phosphatase Ppe1 and Insig in fission yeast. J Biol Chem. 2011;111:233452. Burg JS, Espenshade PJ. Glucose controls phosphoregulation of HMG-CoA reductase through the PP2A-related phosphatase Ppe1 and Insig in fission yeast. J Biol Chem. 2011;111:233452.
49.
go back to reference Mathews EH, Liebenberg L, Pelzer R. High-glycolytic cancers and their interplay with the body’s glucose demand and supply cycle. Med Hypotheses. 2011;76:157–65.CrossRefPubMed Mathews EH, Liebenberg L, Pelzer R. High-glycolytic cancers and their interplay with the body’s glucose demand and supply cycle. Med Hypotheses. 2011;76:157–65.CrossRefPubMed
50.
go back to reference Zhang A, Wu Y, Lai H, Yew D. Apoptosis—a brief review. Neuroembryol Aging. 2005;3:47–59.CrossRef Zhang A, Wu Y, Lai H, Yew D. Apoptosis—a brief review. Neuroembryol Aging. 2005;3:47–59.CrossRef
Metadata
Title
Targeting prostate cancer cell metabolism: impact of hexokinase and CPT-1 enzymes
Authors
Rouhallah Najjar Sadeghi
Fatemeh Karami-Tehrani
Siamak Salami
Publication date
01-04-2015
Publisher
Springer Netherlands
Published in
Tumor Biology / Issue 4/2015
Print ISSN: 1010-4283
Electronic ISSN: 1423-0380
DOI
https://doi.org/10.1007/s13277-014-2919-4

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