Strategie odżywcze komórek nowotworowych – przegląd wybranych typów nowotworów z uwzględnieniem zmian w poziomie i wzorze ekspresji transporterów glukozy

• Autorzy: Gajek K. , Wiatrak B. , Ślęzak A. , Ussowicz M.

Warianty tytułu

EN

Nutritional strategies of tumor cells – review of selected cancer types involving changes of expression level and pattern of glucose

• Języki publikacji: PL

Abstrakty

PL

Zaburzona równowaga pomiędzy proliferacją a dojrzewaniem i różnicowaniem komórek nowotworowych powoduje szybki wzrost guza, prowadząc do zwiększenia zapotrzebowania na składniki odżywcze, m.in. glukozę i tlen. Pierwszą odpowiedzią komórek nowotworowych na niewystarczającą ilość składników odżywczych jest zmiana metabolizmu na beztlenowy (efekt Warburga). Glukoza niezbędna do przeprowadzenia tego procesu dostarczana jest za pomocą transporterów – najczęściej białek GLUT1 i SGLT1. Zmiana poziomu i wzoru ekspresji transporterów glukozy w komórkach nowotworowych w porównaniu z komórkami odpowiednich tkanek prawidłowych świadczy o adaptacji, do której doszło w obrębie guza. Dotychczasowe badania pozwoliły ustalić, w których rodzajach nowotworów dochodzi do zmian w ekspresji białek GLUT1 i SGLT1 oraz pokazały, że zmiany te mogą mieć bezpośredni związek z zaawansowaniem choroby i rokowaniem dla pacjentów. Niniejsza praca ma charakter przeglądowy i stanowi zestawienie zmian w poziomie ekspresji transporterów glukozy w niektórych typach nowotworów. Określenie poziomu ekspresji tych białek w komórkach nowotworowych może mieć kluczowe znaczenie dla spersonalizowanej terapii przeciwnowotworowej.

EN

Due to imbalance between proliferation, differentiation and maturation, cancer cells grow rapidly and require elevated levels of oxygen and glucose. The main strategy of cancer cells is to prevent starvation is the anaerobic adaptation of cellular metabolism known as the Warburg’s effect. Increased glucose uptake is maintained by alterating the level and the pattern of glucose transporters expression, mainly GLUT1 and SGLT1. In many cancer types, these proteins are present despite their absence in healthy tissue. Previous researches revealed cancer types in which GLUT1 and SGLT1 expression are altered. There is a strong direct correlation between their expression pattern, cancer stage and prognosis for the patient. This review provides an overview of changes in the level of glucose transporters expression in some cancer types. Determination of glucose transporters expression levels in cancer cells could be crucial for personalized cancer treatment.

Słowa kluczowe

PL

GLUT1; SGLT1; hipoksja; komórki nowotworowe; transport glukozy

EN

GLUT1; SGLT1; hypoxia; cancer cells; glucose transport

• Wydawca: Jacek Doskocz
• Czasopismo: Acta Bio-Optica et Informatica Medica. Inżynieria Biomedyczna
• Rocznik: 2017
• Tom: Vol. 23, nr 2
• Strony: 133--146
• Opis fizyczny: Bibliogr. 79 poz.

Twórcy

autor

Gajek K.

• Uniwersytet Medyczny im. Piastów Śląskich we Wrocławiu, Katedra i Klinika Transplantacji Szpiku, Onkologii i Hematologii Dziecięcej, 50-556 Wrocław, ul. Borowska 213

autor

Wiatrak B.

• Uniwersytet Medyczny im. Piastów Śląskich we Wrocławiu, Katedra i Zakład Podstaw Nauk Medycznych, 50-556 Wrocław, ul. Borowska 211

autor

Ślęzak A.

• Uniwersytet Medyczny im. Piastów Śląskich we Wrocławiu, Katedra i Zakład Podstaw Nauk Medycznych, 50-556 Wrocław, ul. Borowska 211

autor

Ussowicz M.

• Uniwersytet Medyczny im. Piastów Śląskich we Wrocławiu, Katedra i Klinika Transplantacji Szpiku, Onkologii i Hematologii Dziecięcej, 50-556 Wrocław, ul. Borowska 213

Bibliografia

• [1] J.W. Kim, C.V. Dang: Cancer’s molecular sweet tooth and the warburg effect, Cancer Research, vol. 66(18), 2006, s. 8927–8930.
• [2] M.G. Vander Heiden, L.C. Cantley, C.B. Thompson: Understanding the Warburg effect: the metabolic requirements of cell proliferation, Science, vol. 324(5930), 2009, s. 1029–1033.
• [3] P. Sadłecki, M. Walentowicz-Sadłecka, M. Grabiec: Rola angiogenezy w rozwoju nowotworów, Przegląd Menopauzalny, vol. 14(1), 2010, s. 28–31.
• [4] A. Banyś, L. Bułaś, E. Długosz, B. Szulc-Musiał, A. Jankowski: Angiogeneza w chorobie nowotworowej, Patofizjologia, vol. 65(4), 2009, s. 247–250.
• [5] P. Jarosz, B. Woźniak: Angiogeneza w chorobach nowotworowych, Przegląd Medyczny Uniwersytetu Rzeszowskiego i Narodowego Instytutu Leków w Warszawie, vol. 4, 2012, s. 498–507.
• [6] K.M. Cook, D. Phil, W.D. Figg, D. Pharm: Angiogenesis inhibitors: current strategies and future prospects, CA: A Cancer Journal for Clinicians, vol. 60(4), 2010, s. 222–243.
• [7] A.F. Karamysheva: Mechanisms of Angiogenesis, Biochemistry, vol. 73(7), 2008, s. 751–762.
• [8] R. Oklu, T.G. Walker, S. Wicky, R. Hesketh: Angiogenesis and current antiangiogenic strategies for the treatment of cancer, Journal of Vascular and Interventional Radiology, vol. 21(12), 2010, s. 1791–1805.
• [9] P. Carmeliet: Angiogenesis in health and disease, Nature Medicine, vol. 9(6), 2003, s. 653–660.
• [10] A. Kurzyk: Angiogeneza - możliwości, problemy, perspektywy, Postępy Biochemii, vol. 61(1), 2015, s. 25–34.
• [11] T.M. Zielonka: Angiogeneza - Część I. Mechanizm powstawania nowych naczyń krwionośnych, Alergia Astma Immunologia, vol. 8(4), 2003, s. 169–174.
• [12] J. Skóra, J. Biegus, A. Pupka, P. Barć, J. Sikora, P. Szyber: Molekularne podstawy angiogenezy, Postępy Higieny i Medycyny Doświadczalnej (Online), vol. 60, 2006, s. 410–415.
• [13] J. Gibbons: Angiogenesis: Emerging Roles for the TGFβ Superfamily, Pathways Magazine, vol. 11, 2010, s. 14–16.
• [14] P.J. Höglund, K.J.V Nordström, H.B. Schiöth, R. Fredriksson: The solute carrier families have a remarkably long evolutionary history with the majority of the human families present before divergence of Bilaterian species, Molecular Biology and Evolution, vol. 28(4), 2011, s. 1531–1541.
• [15] H. Joost, G.I. Bell, J.D. Best, M.J. Birnbaum, M.J. Charron, Y.T. Chen, H. Doege, D.E. James, H.F. Lodish, K.H. Moley, J.F. Moley, M. Mueckler, S. Rogers, A. Schürmann, S. Seino, B. Thorens: Nomenclature of the GLUT/SLC2A family of sugar/polyol transport facilitators, American Journal of Physiology − Endocrinology and Metabolism, vol. 282(4), 2002, s. E974–E976.
• [16] I.S. Wood, P. Trayhurn: Glucose transporters (GLUT and SGLT): expanded families of sugar transport proteins, British Journal of Nutrition, vol. 89(1), 2003, s. 3–9.
• [17] L. Szablewski: Expression of glucose transporters in cancers, Biochimica et Biophysica Acta − Reviews on Cancer, vol. 1835(2), 2013, s. 164–169.
• [18] E.M. Wright: Surprising Versatility of Na+-Glucose Cotransporters: SLC5, Physiology, vol. 19(6), 2004, s. 370–376.
• [19] M. Mueckler: Facilitative glucose transporters, European Journal of Biochemistry, vol. 219(3), 1994, s. 713–725.
• [20] F.-Q. Zhao, A.F. Keating: Functional properties and genomics of glucose transporters, Current Genomics, vol. 8(2), 2007, s. 113–128.
• [21] P. Jóźwiak, A. Lipińska: Rola transportera glukozy 1 (GLUT1) w diagnostyce i terapii nowotworów, Postȩpy Higieny i Medycyny Doświadczalnej (Online), vol. 66, 2012, s. 165–174.
• [22] E.M. Wright, D.D.F. Loo, B.A. Hirayama: Biology of human sodium glucose transporters, Physiological Reviews, vol. 91, 2011, s. 733–794.
• [23] N. Samih, S. Hovsepian, F. Notel, M. Prorok, H. Zattara-Cannoni, S. Mathieu, D. Lombardo, G. Fayet, A. El-Battari: The impact of N- and O-glycosylation on the functions of Glut-1 transporter in human thyroid anaplastic cells, Biochimica et Biophysica Acta − General Subjects, vol. 1621(1), 2003, s. 92–101.
• [24] M.C. Maiden, E.O. Davis, S.A. Baldwin, D.C. Moore, P.J. Henderson: Mammalian and bacterial sugar transport proteins are homologous, Nature, vol. 325(6105), 1987, s. 641–643.
• [25] H.L. Wieman, S.R. Horn, S.R. Jacobs, B.J. Altman, S. Kornbluth, J.C. Rathmell: An essential role for the Glut1 PDZbinding motif in growth factor regulation of Glut1 degradation and trafficking, Biochemical Journal, vol. 418(2), 2009, s. 345–367.
• [26] M.J. Seatter, S. a. De La Rue, L.M. Porter, G.W. Gould: QLS motif in transmembrane helix VII of the glucose transporter family interacts with the C-1 position of D-glucose and is involved in substrate selection at the exofacial binding site, Biochemistry, vol. 37(5), 1998, s. 1322–1326.
• [27] E.M. Wright, E. Turk: The sodium/glucose cotransport family SLC5, Pflügers Archiv - European Journal of Physiology, vol. 447(5), 2004, s. 510–518.
• [28] E.M. Wright, J.R. Hirsch, D.D. Loo, G. a Zampighi: Regulation of Na+/glucose cotransporters, Journal of Experimental Biology, vol. 200(Pt 2), 1997, s. 287–293.
• [29] M. Uldry, M. Ibberson, M. Hosokawa, B. Thorens: GLUT2 is a high affinity glucosamine transporter, FEBS Letters, vol. 524(1–3), 2002, s. 199–203.
• [30] J.M. Berg, J.L. Tymoczko, L. Stryer: Biochemia, Wydawnictwo Naukowe PWN, Warszawa 2007.
• [31] R.A. Medina, G.I. Owen: Glucose transporters: expression, regulation and cancer, Biological Research, vol. 35(1), 2002, s. 9–26.
• [32] V.F. Casneuf, P. Fonteyne, N. Van Damme, P. Demetter, P. Pauwels, B. de Hemptinne, M. De Vos, C. Van de Wiele, M. Peeters: Expression of SGLT1, Bcl-2 and p53 in primary pancreatic cancer related to survival, Cancer Investigation, vol. 26(8), 2008, s. 852–859.
• [33] B.M. Helmke, C. Reisser, M. Idzko, G. Dyckhoff, C. Herold-Mende, M. Idzkoe: Expression of SGLT-1 in preneoplastic and neoplastic lesions of the head and neck, Oral Oncology, vol. 40(1), 2004, s. 28–35.
• [34] N. Ishikawa, T. Oguri, T. Isobe, K. Fujitaka, N. Kohno: SGLT Gene Expression in Primary Lung Cancers and Their Metastatic Lesions, Japanese Journal of Cancer Research, vol. 92(8), 2001, s. 874–879.
• 35] V. Ganapathy, M. Thangaraju, P.D. Prasad: Nutrient transporters in cancer: Relevance to Warburg hypothesis and beyond, Pharmacology and Therapeutics, vol. 121(1), 2009, s. 29–40.
• [36] G.L. Semenza: Targeting HIF-1 for cancer therapy, Nature Reviews Cancer, vol. 3(10), 2003, s. 721–732.
• [37] A. Silva, A. Gírio, I. Cebola, C.I. Santos, F. Antunes, J.T. Barata: Intracellular reactive oxygen species are essential for PI3K/Akt/mTOR-dependent IL-7-mediated viability of T-cell acute lymphoblastic leukemia cells, Leukemia, vol. 25(6), 2011, s. 960–967.
• [38] J. Yun, C. Rago, I. Cheong, R. Pagliarini, P. Angenendt, H. Rajagopalan, K. Schmidt, J.K. V Willson, S. Markowitz, S. Zhou, L.A. Diaz, V.E. Velculescu, C. Lengauer, K.W. Kinzler, B. Vogelstein, N. Papadopoulos: Glucose deprivation contributes to the development of KRAS pathway mutations in tumor cells, Science, vol. 325(5947), 2009, s. 1555–1559.
• [39] T. Santalucía, M. Christmann, M.H. Yacoub, N.J. Brand: Hypertrophic agonists induce the binding of c-Fos to an AP-1 site in cardiac myocytes: implications for the expression of GLUT1, Cardiovascular Research, vol. 59(3), 2003, s. 639–648.
• [40] T. Murakami, T. Nishiyama, T. Shirotani, Y. Shinohara, M. Kan, K. Ishii, F. Kanai, S. Nakazuru, Y. Ebina: Identification of two enhancer elements in the gene encoding the type 1 glucose transporter from the mouse which are responsive to serum, growth factor, and oncogenes, Journal of Biological Chemistry, vol. 267(13), 1992, s. 9300–9306.
• [41] R.C. Osthus, H. Shim, S. Kim, Q. Li, R. Reddy, M. Mukherjee, Y. Xu, D. Wonsey, L.A. Lee, C. V Dang: Deregulation of glucose transporter 1 and glycolytic gene expression by c-Myc, Journal of Biological Chemistry, vol. 275(29), 2000, s. 21797–21800.
• [42] N. Normanno, A. De Luca, C. Bianco, L. Strizzi, M. Mancino, M.R. Maiello, A. Carotenuto, G. De Feo, F. Caponigro, D.S. Salomon: Epidermal growth factor receptor (EGFR) signaling in cancer, Gene, vol. 366(1), 2006, s. 2–16.
• [43] Z. Weihua, R. Tsan, W.C. Huang, Q. Wu, C.H. Chiu, I.J. Fidler, M.C. Hung: Survival of cancer cells is maintained by EGFR independent of its kinase activity, Cancer Cell, vol. 13(5), 2008, s. 385–393.
• [44] J. Ren, L.R. Bollu, F. Su, G. Gao, L. Xu, W.-C. Huang, M.-C. Hung, Z. Weihua: EGFR-SGLT1 interaction does not respond to EGFR modulators, but inhibition of SGLT1 sensitizes prostate cancer cells to EGFR tyrosine kinase inhibitors, The Prostate, vol. 73(13), 2013, s. 1453–1461.
• [45] R.S. Brown, R.L. Wahl: Overexpression of Glut-1 glucose transporter in human breast cancer An immunohistochemical study, Cancer, vol. 72(10), 1993, s. 2979–2985.
• [46] M. Younes, L. V. Lechago, J.R. Somoano, M. Mosharaf, J. Lechago: Wide expression of the human erythrocyte glucose transporter Glut1 in human cancers, Cancer Research, vol. 56(5), 1996, s. 1164–1167.
• [47] M. Younes, R.W. Brown, D.R. Mody, L. Fernandez, R. Laucirica: GLUT1 expression in human breast carcinoma: correlation with known prognostic markers, Anticancer Research, vol. 15(6B), 1995, s. 2895–2898.
• [48] S.S. Kang, Y.K. Chun, M.H. Hur, H.K. Lee, Y.J. Kim, S.R. Hong, J.H. Lee, S.G. Lee, Y.K. Park: Clinical significance of glucose transporter 1 (GLUT1) expression in human breast carcinoma, Japanese Journal of Cancer Research, vol. 93(10), 2002, s. 1123–1128.
• [49] Y.R. Hussein, S. Bandyopadhyay, A. Semaan, Q. Ahmed, B. Albashiti, T. Jazaerly, Z. Nahleh, R. Ali-Fehmi: Glut-1 Expression Correlates with Basal-like Breast Cancer, Translational Oncology, vol. 4(6), 2011, s. 321–327.
• [50] S.M. Jang, H. Han, K.-S. Jang, Y.J. Jun, S.-H. Jang, K.-W. Min, M.S. Chung, S.S. Paik: The Glycolytic Phenotype is Correlated with Aggressiveness and Poor Prognosis in Invasive Ductal Carcinomas, Journal of Breast Cancer, vol. 15(2), 2012, s. 172–180.
• [51] K.C. Carvalho, I.W. Cunha, R.M. Rocha, F.R. Ayala, M.M. Cajaíba, M.D. Begnami, R.S. Vilela, G.R. Paiva, R.G. Andrade, F. a Soares: GLUT1 expression in malignant tumors and its use as an immunodiagnostic marker, Clinical Science, vol. 66(6), 2011, s. 965–972.
• [52] A. Godoy, K. Salazar, C. Figueroa, G.J. Smith, M. de los Angeles Garcia, F.J. Nualart: Nutritional channels in breast cancer, Journal of Cellular and Molecular Medicine, vol. 13(9 B), 2009, s. 3973–3984.
• [53] C. Scafoglio, B.A. Hirayama, V. Kepe, J. Liu, C. Ghezzi, N. Satyamurthy, N.A. Moatamed, J. Huang, H. Koepsell, J.R. Barrio, E.M. Wright: Functional expression of sodium-glucose transporters in cancer, Proceedings of the National Academy of Sciences of the United States of America, vol. 112(30), 2015, s. E4111–E4119.
• [54] K. Lu, J. Yang, D. Li, S. He, D. Zhu, L. Zhang, X. Zhang, X. Chen, B. Zhang, J. Zhou: Expression and clinical significance of glucose transporter-1 in pancreatic cancer, Oncology Letters, vol. 12(1), 2016, s. 243–249.
• [55] M.S. Wideł, M. Wideł: Mechanizmy przerzutowania i molekularne markery progresji nowotworów złośliwych. I. Rak jelita grubego, Postępy Higieny i Medycyny Doświadczalnej (Online), vol. 60, 2006, s. 453–470.
• [56] G.F. Guo, Y.C. Cai, B. Zhang, R.H. Xu, H.J. Qiu, L.P. Xia, W.Q. Jiang, P.L. Hu, X.X. Chen, F.F. Zhou, F. Wang: Overexpression of SGLT1 and EGFR in colorectal cancer showing a correlation with the prognosis, Medical Oncology, vol. 28(suppl. 1), 2011, s. S197–S203.
• [57] R.S. Haber, A. Rathan, K.R. Weiser, A. Pritsker, S.H. Itzkowitz, C. Bodian, G. Slater, A. Weiss, D.E. Burstein: GLUT1 glucose transporter expression in colorectal carcinoma, Cancer, vol. 83(1), 1998, s. 34–40.
• [58] A. Furudoi, S. Tanaka, K. Haruma, M. Yoshihara, K. Sumii, G. Kajiyama, F. Shimamoto: Clinical significance of human erythrocyte glucose transporter 1 expression at the deepest invasive site of advanced colorectal carcinoma, Oncology, vol. 60(2), 2001, s. 162–169.
• [59] B. Lai, Y. Xiao, H. Pu, Q. Cao, H. Jing, X. Liu: Overexpression of SGLT1 is correlated with tumor development and poor prognosis of ovarian carcinoma, Archives of Gynecology and Obstetrics, vol. 285(5), 2012, s. 1455–1461.
• [60] M. Tsukioka, Y. Matsumoto, M. Noriyuki, C. Yoshida, H. Nobeyama, H. Yoshida, T. Yasui, T. Sumi, K. Honda, O. Ishiko: Expression of glucose transporters in epithelial ovarian carcinoma: correlation with clinical characteristics and tumor angiogenesis, Oncology Reports, vol. 18(2), 2007, s. 361–367.
• [61] G.E. Bedkowska, S. Ławicki, M. Szmitkowski: Molecular markers of carcinogenesis in the diagnostics of cervical cancer, Postępy Higieny i Medycyny Doświadczalnej (Online), vol. 63, 2009, s. 99–105.
• [62] M. Perez, J.M. Praena-Fernandez, B. Felipe-Abrio, M. a. Lopez-Garcia, A. Lucena-Cacace, A. Garcia, M. Lleonart, G. Roncador, J.J. Marin, A. Carnero: MAP17 and SGLT1 Protein Expression Levels as Prognostic Markers for Cervical Tumor Patient Survival, PLoS ONE, vol. 8(2), 2013, s. 1–10.
• [63] R. Dadej, P. Cieśliński, Z. Kwias: Rak stercza, Współczesna Onkologia, vol. 6(2), 2002, s. 108–116.
• [64] P. Effert, J. Beniers, Y. Tamimi, S. Handt, G. Jakse: Expression of glucose transporter 1 (Glut-1) in cell lines and clinical specimens from human prostate adenocarcinoma, Anticancer Research, vol. 24(5A), 2004, s. 3057–3063.
• [65] J. Jans, J.H. Van Dijk, S. Van Schelven, P. Van Der Groep, S.H. Willems, T.N. Jonges, P.J. Van Diest, J.L.H.R. Bosch: Expression and localization of hypoxia proteins in prostate cancer: prognostic implications after radical prostatectomy, Cancer, vol. 75(4), 2010, s. 786–792.
• [66] A. Blessing, L. Xu, G. Gao, L.R. Bollu, J. Ren, H. Li, X. Wu, F. Su, W.-C. Huang, M.-C. Hung, L. Huo, G.S. Palapattu, Z. Weihua: Sodium/Glucose Co-transporter 1 Expression Increases in Human Diseased Prostate, Journal of Cancer Science & Therapy, vol. 4(9), 2012, s. 306–312.
• [67] Y. Hanabata, Y. Nakajima, K.I. Morita, K. Kayamori, K. Omura: Coexpression of SGLT1 and EGFR is associated with tumor differentiation in oral squamous cell carcinoma, Odontology, vol. 100(2), 2012, s. 156–163.
• [68] T. Nishioka, Y. Oda, Y. Seino, T. Yamamoto, N. Inagaki, H. Yano, H. Imura, R. Shigemoto, H. Kikuchi: Distribution of the glucose transporters in human brain tumors, Cancer Research, vol. 52, 1992, s. 3972–3979.
• [69] R.J. Boado, K.L. Black, W.M. Pardridge: Gene expression of GLUT3 and GLUT1 glucose transporters in human brain tumors, Molecular Brain Research, vol. 27(1), 1994, s. 51–57.
• [70] W.A. Flavahan, Q. Wu, M. Hitomi, N. Rahim, Y. Kim, A.E. Sloan, R.J. Weil, I. Nakano, J.N. Sarkaria, B.W. Stringer, B.W. Day, M. Li, J.D. Lathia, J.N. Rich, A.B. Hjelmeland: Brain tumor initiating cells adapt to restricted nutrition through preferential glucose uptake, Nature Neuroscience, vol. 16(10), 2013, s. 1373–1382.
• [71] J. Lortet-Tieulent, I. Soerjomataram, J. Ferlay, M. Rutherford, E. Weiderpass, F. Bray: International trends in lung cancer incidence by histological subtype: Adenocarcinoma stabilizing in men but still increasing in women, Lung Cancer, vol. 84(1), 2014, s. 13–22.
• [72] T. Kurata, T. Oguri, T. Isobe, S. Ishioka, M. Yamakido: Differential expression of facilitative glucose transporter (GLUT) genes in primary lung cancers and their liver metastases, Japanese Journal of Cancer Research, vol. 90(11), 1999, s. 1238–1243.
• [73] M. Masin, J. Vazquez, S. Rossi, S. Groeneveld, N. Samson, P.C. Schwalie, B. Deplancke, L.E. Frawley, J. Gouttenoire, D. Moradpour, T.G. Oliver, E. Meylan: GLUT3 is induced during epithelial-mesenchymal transition and promotes tumor cell proliferation in non-small cell lung cancer, Cancer & Metabolism, vol. 2(1), 2014, s. 11.
• [74] K. Matsushita, K. Uchida, S. Saigusa, S. Ide, K. Hashimoto, Y. Koike, K. Otake, M. Inoue, K. Tanaka, M. Kusunoki: Glycolysis inhibitors as a potential therapeutic option to treat aggressive neuroblastoma expressing GLUT1, Journal of Pediatric Surgery, vol. 47(7), 2012, s. 1323–1330.
• [75] E. Adamkiewicz-Drożyńska: Czynniki prognostyczne i nowe możliwości leczenia neuroblastoma, Współczesna Onkologia, vol. 4(2), 2000, s. 72–75.
• [76] V.C. Russo, K. Kobayashi, S. Najdovska, N.L. Baker, G.A. Werther: Neuronal protection from glucose deprivation via modulation of glucose transport and inhibition of apoptosis: a role for the insulin-like growth factor system, Brain Research, vol. 1009(1–2), 2004, s. 40–53.
• [77] B. Fang, J. Jia: Human neuroblastoma cells transfected with two Chinese presenilin 1 mutations are sensitized to trophic factor withdrawal and protected by insulin-like growth factor-1, Chinese Medical Journal, vol. 121(10), 2008, s. 910–915.
• [78] K. Matsushita, K. Uchida, S. Saigusa, S. Ide, K. Hashimoto, Y. Koike, K. Otake, M. Inoue, K. Tanaka, M. Kusunoki: Glycolysis inhibitors as a potential therapeutic option to treat aggressive neuroblastoma expressing GLUT1, Journal of Pediatric Surgery, vol. 47(7), 2012, s. 1323–1330.
• [79] P. Ramani, A. Headford, M.T. May: GLUT1 protein expression correlates with unfavourable histologic category and high risk in patients with neuroblastic tumours, Virchows Archiv, vol. 462(2), 2013, s. 203–209.