Mechanisms of Metastasis and Cell Mobility – The Role of Metabolism

Carsten Gründker; Matthias Läsche; Johanna W. Hellinger; Günter Emons

doi:10.1055/a-0805-9113

Geburtshilfe und Frauenheilkunde, Inhaltsverzeichnis

Geburtshilfe Frauenheilkd 2019; 79(02): 184-188
DOI: 10.1055/a-0805-9113

GebFra Science

Review/Übersicht

Georg Thieme Verlag KG Stuttgart · New York

Mechanisms of Metastasis and Cell Mobility – The Role of Metabolism

Artikel in mehreren Sprachen: English | deutsch

Authors

Carsten Gründker

Universitätsmedizin Göttingen, Klinik für Gynäkologie und Geburtshilfe, Göttingen, Germany
Matthias Läsche

Universitätsmedizin Göttingen, Klinik für Gynäkologie und Geburtshilfe, Göttingen, Germany
Johanna W. Hellinger

Universitätsmedizin Göttingen, Klinik für Gynäkologie und Geburtshilfe, Göttingen, Germany
Günter Emons

Universitätsmedizin Göttingen, Klinik für Gynäkologie und Geburtshilfe, Göttingen, Germany

Abstract

Tumour metastasis is responsible for more than 90% of tumour-associated mortality. About one third of breast cancer patients in the early stage develop metastases. The transformation in tumour development referred to as the “metastatic cascade” or “metastatic cycle” is a complex and multi-stage event. While it is generally recognised that epithelial-mesenchymal transformation (EMT) plays a crucial role in cancer progression and metastasis, the metabolic events in this process have received little attention to date. We would therefore like to provide a brief overview here of the influence of the metabolism on the progression and metastasis of tumours.

Key words

breast cancer - metastasis - metabolism - aerobic glycolysis

Volltext

Referenzen

References/Literatur
1 Berg JM, Stryer L, Tymoczko JL. et al. Biochemistry. New York: WH Freeman; 2015
2 Nordstrom L, Achanna S, Naka K. et al. Fetal and maternal lactate increase during active second stage of labour. BJOG 2001; 108: 263-268
3 Ward PS, Thompson CB. Metabolic reprogramming: a cancer hallmark even warburg did not anticipate. Cancer Cell 2012; 21: 297-308
4 Warburg O. Über den Stoffwechsel der Carcinomzelle. Naturwissenschaften 1924; 12: 1131-1137
5 Warburg O, Wind F, Negelein E. THE METABOLISM OF TUMORS IN THE BODY. J Gen Physiol 1927; 8: 519-530
6 Marin-Hernandez A, Gallardo-Perez JC, Hernandez-Resendiz I. et al. Hypoglycemia Enhances Epithelial-Mesenchymal Transition and Invasiveness, and Restrains the Warburg Phenotype, in Hypoxic HeLa Cell Cultures and Microspheroids. J Cell Physiol 2017; 232: 1346-1359
7 Warburg O. On the origin of cancer cells. Science 1956; 123: 309-314
8 Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation. Cell 2011; 144: 646-674
9 Koivunen P, Lee S, Duncan CG. et al. Transformation by the (R)-enantiomer of 2-hydroxyglutarate linked to EGLN activation. Nature 2012; 483: 484-488
10 Xu W, Yang H, Liu Y. et al. Oncometabolite 2-hydroxyglutarate is a competitive inhibitor of alpha-ketoglutarate-dependent dioxygenases. Cancer Cell 2011; 19: 17-30
11 Guo J, Wang B, Fu Z. et al. Hypoxic Microenvironment Induces EMT and Upgrades Stem-Like Properties of Gastric Cancer Cells. Technol Cancer Res Treat 2016; 15: 60-68
12 Matsuoka J, Yashiro M, Doi Y. et al. Hypoxia stimulates the EMT of gastric cancer cells through autocrine TGFbeta signaling. PLoS One 2013; 8: e62310
13 Shen X, Xue Y, Si Y. et al. The unfolded protein response potentiates epithelial-to-mesenchymal transition (EMT) of gastric cancer cells under severe hypoxic conditions. Med Oncol 2015; 32: 447
14 Zhang H, Sun L, Xiao X. et al. Kruppel-like factor 8 contributes to hypoxia-induced MDR in gastric cancer cells. Cancer Sci 2014; 105: 1109-1115
15 Zhou J, Li K, Gu Y. et al. Transcriptional up-regulation of RhoE by hypoxia-inducible factor (HIF)-1 promotes epithelial to mesenchymal transition of gastric cancer cells during hypoxia. Biochem Biophys Res Commun 2011; 415: 348-354
16 Cairns RA, Harris IS, Mak TW. Regulation of cancer cell metabolism. Nat Rev Cancer 2011; 11: 85-95
17 Pfeiffer T, Schuster S, Bonhoeffer S. Cooperation and competition in the evolution of ATP-producing pathways. Science 2001; 292: 504-507
18 Dai C, Sun F, Zhu C. et al. Tumor environmental factors glucose deprivation and lactic acidosis induce mitotic chromosomal instability–an implication in aneuploid human tumors. PLoS One 2013; 8: e63054
19 Wu H, Ding Z, Hu D. et al. Central role of lactic acidosis in cancer cell resistance to glucose deprivation-induced cell death. J Pathol 2012; 227: 189-199
20 Xie J, Wu H, Dai C. et al. Beyond Warburg effect–dual metabolic nature of cancer cells. Sci Rep 2014; 4: 4927
21 Eckert MA, Santiago-Medina M, Lwin TM. et al. ADAM12 induction by Twist1 promotes tumor invasion and metastasis via regulation of invadopodia and focal adhesions. J Cell Sci 2017; 130: 2036-2048
22 Shi L, Pan H, Liu Z. et al. Roles of PFKFB3 in cancer. Signal Transduct Target Ther 2017; 2: 17044
23 Draoui N, de Zeeuw P, Carmeliet P. Angiogenesis revisited from a metabolic perspective: role and therapeutic implications of endothelial cell metabolism. Open Biol 2017; 7: pii:170219
24 Hu X, Chao M, Wu H. Central role of lactate and proton in cancer cell resistance to glucose deprivation and its clinical translation. Signal Transduct Target Ther 2017; 2: 16047
25 Liang J, Shao SH, Xu ZX. et al. The energy sensing LKB1-AMPK pathway regulates p27(kip1) phosphorylation mediating the decision to enter autophagy or apoptosis. Nat Cell Biol 2007; 9: 218-224
26 Schild T, Low V, Blenis J. et al. Unique Metabolic Adaptations Dictate Distal Organ-Specific Metastatic Colonization. Cancer Cell 2018; 33: 347-354
27 Lopez-Soto A, Gonzalez S, Smyth MJ. et al. Control of Metastasis by NK Cells. Cancer Cell 2017; 32: 135-154
28 Nieto MA, Huang RY, Jackson RA. et al. EMT: 2016. Cell 2016; 166: 21-45
29 Brabletz T, Kalluri R, Nieto MA. et al. EMT in cancer. Nat Rev Cancer 2018; 18: 128-134
30 Pastushenko I, Brisebarre A, Sifrim A. et al. Identification of the tumour transition states occurring during EMT. Nature 2018; 556: 463-468
31 Thompson EW, Nagaraj SH. Transition states that allow cancer to spread. Nature 2018; 556: 442-444
32 Polasik A, Tzschaschel M, Schochter F. et al. Circulating Tumour Cells, Circulating Tumour DNA and Circulating MicroRNA in Metastatic Breast Carcinoma – What is the Role of Liquid Biopsy in Breast Cancer?. Geburtsh Frauenheilk 2017; 77: 1291-1298
33 Massague J, Obenauf AC. Metastatic colonization by circulating tumour cells. Nature 2016; 529: 298-306
34 Obenauf AC, Massague J. Surviving at a Distance: Organ-Specific Metastasis. Trends Cancer 2015; 1: 76-91
35 Mathew A, Rajagopal PS, Villgran V. et al. Distinct Pattern of Metastases in Patients with Invasive Lobular Carcinoma of the Breast. Geburtsh Frauenheilk 2017; 77: 660-666
36 Lehuede C, Dupuy F, Rabinovitch R. et al. Metabolic Plasticity as a Determinant of Tumor Growth and Metastasis. Cancer Res 2016; 76: 5201-5208
37 Zhu A, Lee D, Shim H. Metabolic positron emission tomography imaging in cancer detection and therapy response. Semin Oncol 2011; 38: 55-69
38 Zhu A, Shim H. Current molecular imaging positron emitting radiotracers in oncology. Nucl Med Mol Imaging 2011; 45: 1-14
39 Mazurek S, Boschek CB, Hugo F. et al. Pyruvate kinase type M2 and its role in tumor growth and spreading. Semin Cancer Biol 2005; 15: 300-308
40 Dong G, Mao Q, Xia W. et al. PKM2 and cancer: The function of PKM2 beyond glycolysis. Oncol Lett 2016; 11: 1980-1986
41 He X, Du S, Lei T. et al. PKM2 in carcinogenesis and oncotherapy. Oncotarget 2017; 8: 110656-110670
42 Vander Heiden MG. Targeting cancer metabolism: a therapeutic window opens. Nat Rev Drug Discov 2011; 10: 671-684
43 Luengo A, Gui DY, Vander Heiden MG. Targeting Metabolism for Cancer Therapy. Cell Chem Biol 2017; 24: 1161-1180
44 Taran FA, Schneeweiss A, Lux MP. et al. Update Breast Cancer 2018 (Part 1) – Primary Breast Cancer and Biomarkers. Geburtsh Frauenheilk 2018; 78: 237-245
45 Schneeweiss A, Lux MP, Janni W. et al. Update Breast Cancer 2018 (Part 2) – Advanced Breast Cancer, Quality of Life and Prevention. Geburtsh Frauenheilk 2018; 78: 246-259