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Breast Cancer Research
Published in: Breast Cancer Research 1/2016

Open Access 01-12-2016 | Review

Cancer stem cell metabolism

Authors: Maria Peiris-Pagès, Ubaldo E. Martinez-Outschoorn, Richard G. Pestell, Federica Sotgia, Michael P. Lisanti

Published in: Breast Cancer Research | Issue 1/2016

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Abstract

Cancer is now viewed as a stem cell disease. There is still no consensus on the metabolic characteristics of cancer stem cells, with several studies indicating that they are mainly glycolytic and others pointing instead to mitochondrial metabolism as their principal source of energy. Cancer stem cells also seem to adapt their metabolism to microenvironmental changes by conveniently shifting energy production from one pathway to another, or by acquiring intermediate metabolic phenotypes. Determining the role of cancer stem cell metabolism in carcinogenesis has become a major focus in cancer research, and substantial efforts are conducted towards discovering clinical targets.
Literature
1.
Aguilar-Gallardo C, Simon C. Cells, stem cells, and cancer stem cells. Semin Reprod Med. 2013;31(1):5–13.CrossRefPubMed
2.
3.
Brooks MD, Burness ML, Wicha MS. Therapeutic implications of cellular heterogeneity and plasticity in breast cancer. Cell Stem Cell. 2015;17(3):260–71.CrossRefPubMedPubMedCentral
4.
5.
Lagadec C, Meignan S, Adriaenssens E, Foveau B, Vanhecke E, Romon R, et al. TrkA overexpression enhances growth and metastasis of breast cancer cells. Oncogene. 2009;28(18):1960–70.CrossRefPubMed
6.
Guppy M, Greiner E, Brand K. The role of the Crabtree effect and an endogenous fuel in the energy metabolism of resting and proliferating thymocytes. Eur J Biochem. 1993;212(1):95–9.CrossRefPubMed
7.
Zhou W, Choi M, Margineantu D, Margaretha L, Hesson J, Cavanaugh C, et al. HIF1alpha induced switch from bivalent to exclusively glycolytic metabolism during ESC-to-EpiSC/hESC transition. Embo J. 2012;31(9):2103–16.CrossRefPubMedPubMedCentral
8.
Folmes CD, Nelson TJ, Martinez-Fernandez A, Arrell DK, Lindor JZ, Dzeja PP, et al. Somatic oxidative bioenergetics transitions into pluripotency-dependent glycolysis to facilitate nuclear reprogramming. Cell Metab. 2011;14(2):264–71.CrossRefPubMedPubMedCentral
9.
Jang H, Yang J, Lee E, Cheong JH. Metabolism in embryonic and cancer stemness. Arch Pharm Res. 2015;38(3):381–8.CrossRefPubMed
10.
Prigione A, Fauler B, Lurz R, Lehrach H, Adjaye J. The senescence-related mitochondrial/oxidative stress pathway is repressed in human induced pluripotent stem cells. Stem Cells. 2010;28(4):721–33.CrossRefPubMed
11.
Jang YY, Sharkis SJ. A low level of reactive oxygen species selects for primitive hematopoietic stem cells that may reside in the low-oxygenic niche. Blood. 2007;110(8):3056–63.CrossRefPubMedPubMedCentral
12.
Liu PP, Liao J, Tang ZJ, Wu WJ, Yang J, Zeng ZL, et al. Metabolic regulation of cancer cell side population by glucose through activation of the Akt pathway. Cell Death Differ. 2012;21(1):124–35.CrossRef
13.
Dando I, Dalla Pozza E, Biondani G, Cordani M, Palmieri M, Donadelli M. The metabolic landscape of cancer stem cells. IUBMB Life. 2015;67(9):687–93.CrossRefPubMed
14.
Ciavardelli D, Rossi C, Barcaroli D, Volpe S, Consalvo A, Zucchelli M, et al. Breast cancer stem cells rely on fermentative glycolysis and are sensitive to 2-deoxyglucose treatment. Cell Death Dis. 2014;5:e1336.CrossRefPubMedPubMedCentral
15.
Emmink BL, Verheem A, Van Houdt WJ, Steller EJ, Govaert KM, Pham TV, et al. The secretome of colon cancer stem cells contains drug-metabolizing enzymes. J Proteomics. 2013;91:84–96.CrossRefPubMed
16.
Liao J, Qian F, Tchabo N, Mhawech-Fauceglia P, Beck A, Qian Z, et al. Ovarian cancer spheroid cells with stem cell-like properties contribute to tumor generation, metastasis and chemotherapy resistance through hypoxia-resistant metabolism. PLoS One. 2014;9(1):e84941.CrossRefPubMedPubMedCentral
17.
Palorini R, Votta G, Balestrieri C, Monestiroli A, Olivieri S, Vento R, et al. Energy metabolism characterization of a novel cancer stem cell-like line 3AB-OS. J Cell Biochem. 2014;115(2):368–79.CrossRefPubMed
18.
Zhou Y, Zhou Y, Shingu T, Feng L, Chen Z, Ogasawara M, et al. Metabolic alterations in highly tumorigenic glioblastoma cells: preference for hypoxia and high dependency on glycolysis. J Biol Chem. 2011;286(37):32843–53.CrossRefPubMedPubMedCentral
19.
Guha M, Srinivasan S, Ruthel G, Kashina AK, Carstens RP, Mendoza A, et al. Mitochondrial retrograde signaling induces epithelial-mesenchymal transition and generates breast cancer stem cells. Oncogene. 2013;33(45):5238–50.CrossRefPubMedPubMedCentral
20.
Petros JA, Baumann AK, Ruiz-Pesini E, Amin MB, Sun CQ, Hall J, et al. mtDNA mutations increase tumorigenicity in prostate cancer. Proc Natl Acad Sci U S A. 2005;102(3):719–24.CrossRefPubMedPubMedCentral
21.
Wang C, Li Z, Lu Y, Du R, Katiyar S, Yang J, et al. Cyclin D1 repression of nuclear respiratory factor 1 integrates nuclear DNA synthesis and mitochondrial function. Proc Natl Acad Sci U S A. 2006;103(31):11567–72.CrossRefPubMedPubMedCentral
22.
Sakamaki T, Casimiro MC, Ju X, Quong AA, Katiyar S, Liu M, et al. Cyclin D1 determines mitochondrial function in vivo. Mol Cell Biol. 2006;26(14):5449–69.CrossRefPubMedPubMedCentral
23.
Lee WT, St John J. The control of mitochondrial DNA replication during development and tumorigenesis. Ann N Y Acad Sci. 2015;1350:95–106.CrossRefPubMed
24.
De Luca A, Fiorillo M, Peiris-Pages M, Ozsvari B, Smith DL, Sanchez-Alvarez R, et al. Mitochondrial biogenesis is required for the anchorage-independent survival and propagation of stem-like cancer cells. Oncotarget. 2015;6(17):14777–95.CrossRefPubMedPubMedCentral
25.
Janiszewska M, Suva ML, Riggi N, Houtkooper RH, Auwerx J, Clement-Schatlo V, et al. Imp2 controls oxidative phosphorylation and is crucial for preserving glioblastoma cancer stem cells. Genes Dev. 2012;26(17):1926–44.CrossRefPubMedPubMedCentral
26.
Lagadinou ED, Sach A, Callahan K, Rossi RM, Neering SJ, Minhajuddin M, et al. BCL-2 inhibition targets oxidative phosphorylation and selectively eradicates quiescent human leukemia stem cells. Cell Stem Cell. 2013;12(3):329–41.CrossRefPubMedPubMedCentral
27.
Lamb R, Bonuccelli G, Ozsvari B, Peiris-Pages M, Fiorillo M, Smith DL, et al. Mitochondrial mass, a new metabolic biomarker for stem-like cancer cells: understanding WNT/FGF-driven anabolic signaling. Oncotarget. 2015;6(31):30453–71.PubMedPubMedCentral
28.
Pasto A, Bellio C, Pilotto G, Ciminale V, Silic-Benussi M, Guzzo G, et al. Cancer stem cells from epithelial ovarian cancer patients privilege oxidative phosphorylation, and resist glucose deprivation. Oncotarget. 2014;5(12):4305–19.CrossRefPubMedPubMedCentral
29.
Sancho P, Burgos-Ramos E, Tavera A, Bou Kheir T, Jagust P, Schoenhals M, et al. MYC/PGC-1alpha balance determines the metabolic phenotype and plasticity of pancreatic cancer stem cells. Cell Metab. 2015;22(4):590–605.CrossRefPubMed
30.
Vlashi E, Lagadec C, Vergnes L, Reue K, Frohnen P, Chan M, et al. Metabolic differences in breast cancer stem cells and differentiated progeny. Breast Cancer Res Treat. 2014;146(3):525–34.CrossRefPubMedPubMedCentral
31.
Farnie G, Sotgia F, Lisanti MP. High mitochondrial mass identifies a sub-population of stem-like cancer cells that are chemo-resistant. Oncotarget. 2015;6(31):30472–86.PubMedPubMedCentral
32.
LeBleu VS, O’Connell JT, Gonzalez Herrera KN, Wikman H, Pantel K, Haigis MC, et al. PGC-1alpha mediates mitochondrial biogenesis and oxidative phosphorylation in cancer cells to promote metastasis. Nat Cell Biol. 2014;16(10):992–1003. 1–15.CrossRefPubMedPubMedCentral
33.
Wey A, Knoepfler PS. c-myc and N-myc promote active stem cell metabolism and cycling as architects of the developing brain. Oncotarget. 2010;1(2):120–30.CrossRefPubMedPubMedCentral
34.
Vazquez F, Lim JH, Chim H, Bhalla K, Girnun G, Pierce K, et al. PGC1alpha expression defines a subset of human melanoma tumors with increased mitochondrial capacity and resistance to oxidative stress. Cancer Cell. 2013;23(3):287–301.CrossRefPubMedPubMedCentral
35.
Yajima T, Ochiai H, Uchiyama T, Takano N, Shibahara T, Azuma T. Resistance to cytotoxic chemotherapy-induced apoptosis in side population cells of human oral squamous cell carcinoma cell line Ho-1-N-1. Int J Oncol. 2009;35(2):273–80.PubMed
36.
Diehn M, Cho RW, Lobo NA, Kalisky T, Dorie MJ, Kulp AN, et al. Association of reactive oxygen species levels and radioresistance in cancer stem cells. Nature. 2009;458(7239):780–3.CrossRefPubMedPubMedCentral
37.
Cipolleschi MG, Marzi I, Santini R, Fredducci D, Vinci MC, D’Amico M, et al. Hypoxia-resistant profile implies vulnerability of cancer stem cells to physiological agents, which suggests new therapeutic targets. Cell Cycle. 2014;13(2):268–78.CrossRefPubMed
38.
Yuan S, Lu Y, Yang J, Chen G, Kim S, Feng L, et al. Metabolic activation of mitochondria in glioma stem cells promotes cancer development through a reactive oxygen species-mediated mechanism. Stem Cell Res Ther. 2015;6(1):198.CrossRefPubMedPubMedCentral
39.
Piskounova E, Agathocleous M, Murphy MM, Hu Z, Huddlestun SE, Zhao Z, et al. Oxidative stress inhibits distant metastasis by human melanoma cells. Nature. 2015;527(7577):186–91.CrossRefPubMedPubMedCentral
40.
Katajisto P, Dohla J, Chaffer CL, Pentinmikko N, Marjanovic N, Iqbal S, et al. Stem cells. Asymmetric apportioning of aged mitochondria between daughter cells is required for stemness. Science. 2015;348(6232):340–3.CrossRefPubMedPubMedCentral
41.
Xie Q, Wu Q, Horbinski CM, Flavahan WA, Yang K, Zhou W, et al. Mitochondrial control by DRP1 in brain tumor initiating cells. Nat Neurosci. 2015;18(4):501–10.CrossRefPubMedPubMedCentral
42.
Biasutto L, Dong LF, Zoratti M, Neuzil J. Mitochondrially targeted anti-cancer agents. Mitochondrion. 2010;10(6):670–81.CrossRefPubMed
43.
Roesch A, Vultur A, Bogeski I, Wang H, Zimmermann KM, Speicher D, et al. Overcoming intrinsic multidrug resistance in melanoma by blocking the mitochondrial respiratory chain of slow-cycling JARID1B(high) cells. Cancer Cell. 2013;23(6):811–25.CrossRefPubMed
44.
Lamb R, Ozsvari B, Lisanti CL, Tanowitz HB, Howell A, Martinez-Outschoorn UE, et al. Antibiotics that target mitochondria effectively eradicate cancer stem cells, across multiple tumor types: treating cancer like an infectious disease. Oncotarget. 2015;6(7):4569–84.CrossRefPubMedPubMedCentral
45.
Jung JW, Park SB, Lee SJ, Seo MS, Trosko JE, Kang KS. Metformin represses self-renewal of the human breast carcinoma stem cells via inhibition of estrogen receptor-mediated OCT4 expression. PLoS One. 2011;6(11):e28068.CrossRefPubMedPubMedCentral
46.
Mayer MJ, Klotz LH, Venkateswaran V. Metformin and prostate cancer stem cells: a novel therapeutic target. Prostate Cancer Prostatic Dis. 2015;18(4):303–9.CrossRefPubMed
47.
Goh J, Enns L, Fatemie S, Hopkins H, Morton J, Pettan-Brewer C, et al. Mitochondrial targeted catalase suppresses invasive breast cancer in mice. BMC Cancer. 2011;11:191.CrossRefPubMedPubMedCentral
48.
Porporato PE, Payen VL, Perez-Escuredo J, De Saedeleer CJ, Danhier P, Copetti T, et al. A mitochondrial switch promotes tumor metastasis. Cell Rep. 2014;8(3):754–66.CrossRefPubMed
49.
Zimorski V, Ku C, Martin WF, Gould SB. Endosymbiotic theory for organelle origins. Curr Opin Microbiol. 2014;22:38–48.CrossRefPubMed
50.
Lamb R, Harrison H, Hulit J, Smith DL, Lisanti MP, Sotgia F. Mitochondria as new therapeutic targets for eradicating cancer stem cells: quantitative proteomics and functional validation via MCT1/2 inhibition. Oncotarget. 2014;5(22):11029–37.CrossRefPubMedPubMedCentral
51.
An H, Kim JY, Oh E, Lee N, Cho Y, Seo JH. Salinomycin promotes anoikis and decreases the CD44+/CD24– stem-like population via inhibition of STAT3 activation in MDA-MB-231 cells. PLoS One. 2015;10(11):e0141919.CrossRefPubMedPubMedCentral
52.
Ferreri AJ, Ponzoni M, Guidoboni M, Resti AG, Politi LS, Cortelazzo S, et al. Bacteria-eradicating therapy with doxycycline in ocular adnexal MALT lymphoma: a multicenter prospective trial. J Natl Cancer Inst. 2006;98(19):1375–82.CrossRefPubMed
53.
Chu DJ, Yao DE, Zhuang YF, Hong Y, Zhu XC, Fang ZR, et al. Azithromycin enhances the favorable results of paclitaxel and cisplatin in patients with advanced non-small cell lung cancer. Genet Mol Res. 2014;13(2):2796–805.CrossRefPubMed
54.
Zhou J, Li P, Xue X, He S, Kuang Y, Zhao H, et al. Salinomycin induces apoptosis in cisplatin-resistant colorectal cancer cells by accumulation of reactive oxygen species. Toxicol Lett. 2013;222(2):139–45.CrossRefPubMed
55.
Gupta PB, Onder TT, Jiang G, Tao K, Kuperwasser C, Weinberg RA, et al. Identification of selective inhibitors of cancer stem cells by high-throughput screening. Cell. 2009;138(4):645–59.CrossRefPubMedPubMedCentral
56.
Vlashi E, Lagadec C, Vergnes L, Matsutani T, Masui K, Poulou M, et al. Metabolic state of glioma stem cells and nontumorigenic cells. Proc Natl Acad Sci U S A. 2011;108(38):16062–7.CrossRefPubMedPubMedCentral
57.
Feng W, Gentles A, Nair RV, Huang M, Lin Y, Lee CY, et al. Targeting unique metabolic properties of breast tumor initiating cells. Stem Cells. 2014;32(7):1734–45.CrossRefPubMedPubMedCentral
58.
Flavahan WA, Wu Q, Hitomi M, Rahim N, Kim Y, Sloan AE, et al. Brain tumor initiating cells adapt to restricted nutrition through preferential glucose uptake. Nat Neurosci. 2013;16(10):1373–82.CrossRefPubMedPubMedCentral
59.
Dong C, Yuan T, Wu Y, Wang Y, Fan TW, Miriyala S, et al. Loss of FBP1 by Snail-mediated repression provides metabolic advantages in basal-like breast cancer. Cancer Cell. 2013;23(3):316–31.CrossRefPubMedPubMedCentral
60.
Gordon N, Skinner AM, Pommier RF, Schillace RV, O’Neill S, Peckham JL, et al. Gene expression signatures of breast cancer stem and progenitor cells do not exhibit features of Warburg metabolism. Stem Cell Res Ther. 2015;6:157.CrossRefPubMedPubMedCentral
61.
Conley SJ, Gheordunescu E, Kakarala P, Newman B, Korkaya H, Heath AN, et al. Antiangiogenic agents increase breast cancer stem cells via the generation of tumor hypoxia. Proc Natl Acad Sci U S A. 2012;109(8):2784–9.CrossRefPubMedPubMedCentral
62.
63.
Sehl ME, Shimada M, Landeros A, Lange K, Wicha MS. Modeling of cancer stem cell state transitions predicts therapeutic response. PLoS One. 2015;10(9):e0135797.CrossRefPubMedPubMedCentral
64.
Conley SJ, Baker TL, Burnett JP, Theisen RL, Lazarus D, Peters CG, et al. CRLX101, an investigational camptothecin-containing nanoparticle-drug conjugate, targets cancer stem cells and impedes resistance to antiangiogenic therapy in mouse models of breast cancer. Breast Cancer Res Treat. 2015;150(3):559–67.CrossRefPubMed
65.
Viale A, Pettazzoni P, Lyssiotis CA, Ying H, Sanchez N, Marchesini M, et al. Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. Nature. 2014;514(7524):628–32.CrossRefPubMedPubMedCentral
66.
Dupuy F, Tabaries S, Andrzejewski S, Dong Z, Blagih J, Annis MG, et al. PDK1-dependent metabolic reprogramming dictates metastatic potential in breast cancer. Cell Metab. 2015;22(4):577–89.CrossRefPubMed
67.
Gammon L, Biddle A, Heywood HK, Johannessen AC, Mackenzie IC. Sub-sets of cancer stem cells differ intrinsically in their patterns of oxygen metabolism. PLoS One. 2013;8(4):e62493.CrossRefPubMedPubMedCentral
68.
Liu S, Cong Y, Wang D, Sun Y, Deng L, Liu Y, et al. Breast cancer stem cells transition between epithelial and mesenchymal states reflective of their normal counterparts. Stem Cell Reports. 2013;2(1):78–91.CrossRefPubMedPubMedCentral
69.
Tamada M, Nagano O, Tateyama S, Ohmura M, Yae T, Ishimoto T, et al. Modulation of glucose metabolism by CD44 contributes to antioxidant status and drug resistance in cancer cells. Cancer Res. 2012;72(6):1438–48.CrossRefPubMed
70.
Nie S, McDermott SP, Deol Y, Tan Z, Wicha MS, Lubman DM. A quantitative proteomics analysis of MCF7 breast cancer stem and progenitor cell populations. Proteomics. 2015;15(22):3772–83.CrossRefPubMedPubMedCentral
71.
Cheong JH, Park ES, Liang J, Dennison JB, Tsavachidou D, Nguyen-Charles C, et al. Dual inhibition of tumor energy pathway by 2-deoxyglucose and metformin is effective against a broad spectrum of preclinical cancer models. Mol Cancer Ther. 2011;10(12):2350–62.CrossRefPubMedPubMedCentral
72.
Creighton CJ, Fu X, Hennessy BT, Casa AJ, Zhang Y, Gonzalez-Angulo AM, Lluch A, Gray JW, Brown PH, Hilsenbeck SG, et al. Proteomic and transcriptomic profiling reveals a link between the PI3K pathway and lower estrogen-receptor (ER) levels and activity in ER+ breast cancer. Breast Cancer Res 2010. 12(3):R40.CrossRefPubMedPubMedCentral
73.
Dave B, Migliaccio I, Gutierrez MC, Wu MF, Chamness GC, Wong H, Narasanna A, Chakrabarty A, Hilsenbeck SG, Huang J, et al. Loss of phosphatase and tensin homolog or phosphoinositol-3 kinase activation and response to trastuzumab or lapatinib in human epidermal growth factor receptor 2-overexpressing locally advanced breast cancers. J Clin Oncol 2011. 29(2):166–173.CrossRefPubMed
74.
Fabi A, Metro G, Di Benedetto A, Nistico C, Vici P, Melucci E, Antoniani B, Perracchio L, Sperduti I, Milella M, et al. Clinical significance of PTEN and p-Akt co-expression in HER2-positive metastatic breast cancer patients treated with trastuzumab-based therapies. Oncology 2010. 78(2):141–149.CrossRefPubMed
75.
Park YH, Jung HA, Choi MK, Chang W, Choi YL, Do IG, Ahn JS, Im YH. Role of HER3 expression and PTEN loss in patients with HER2-overexpressing metastatic breast cancer (MBC) who received taxane plus trastuzumab treatment. Br J Cancer 2014. 110(2):384–391.CrossRefPubMed
76.
Foulkes WD, Stefansson IM, Chappuis PO, Begin LR, Goffin JR, Wong N, Trudel M, Akslen LA. Germline BRCA1 mutations and a basal epithelial phenotype in breast cancer. J Natl Cancer Inst. 2003;95(19):1482–1485.CrossRefPubMed
77.
Chiavarina B, Whitaker-Menezes D, Migneco G, Martinez-Outschoorn UE, Pavlides S, Howell A, et al. HIF1-alpha functions as a tumor promoter in cancer associated fibroblasts, and as a tumor suppressor in breast cancer cells: autophagy drives compartment-specific oncogenesis. Cell Cycle. 2010;9(17):3534–51.CrossRefPubMedPubMedCentral
78.
Chiavarina B, Martinez-Outschoorn UE, Whitaker-Menezes D, Howell A, Tanowitz HB, Pestell RG, et al. Metabolic reprogramming and two-compartment tumor metabolism: opposing role(s) of HIF1alpha and HIF2alpha in tumor-associated fibroblasts and human breast cancer cells. Cell Cycle. 2012;11(17):3280–9.CrossRefPubMedPubMedCentral
79.
Guido C, Whitaker-Menezes D, Capparelli C, Balliet R, Lin Z, Pestell RG, et al. Metabolic reprogramming of cancer-associated fibroblasts by TGF-beta drives tumor growth: connecting TGF-beta signaling with ‘Warburg-like’ cancer metabolism and L-lactate production. Cell Cycle. 2012;11(16):3019–35.CrossRefPubMedPubMedCentral
80.
Martinez-Outschoorn UE, Prisco M, Ertel A, Tsirigos A, Lin Z, Pavlides S, et al. Ketones and lactate increase cancer cell ‘stemness’, driving recurrence, metastasis and poor clinical outcome in breast cancer: achieving personalized medicine via metabolo-genomics. Cell Cycle. 2011;10(8):1271–86.CrossRefPubMedPubMedCentral
81.
82.
Bhowmik SK, Ramirez-Pena E, Arnold JM, Putluri V, Sphyris N, Michailidis G, et al. EMT-induced metabolite signature identifies poor clinical outcome. Oncotarget. 2015;6(40):42651–60.PubMedPubMedCentral
83.
Bonuccelli G, Tsirigos A, Whitaker-Menezes D, Pavlides S, Pestell RG, Chiavarina B, et al. Ketones and lactate ‘fuel’ tumor growth and metastasis: evidence that epithelial cancer cells use oxidative mitochondrial metabolism. Cell Cycle. 2010;9(17):3506–14.CrossRefPubMedPubMedCentral
84.
Pasquier J, Guerrouahen BS, Al Thawadi H, Ghiabi P, Maleki M, Abu-Kaoud N, et al. Preferential transfer of mitochondria from endothelial to cancer cells through tunneling nanotubes modulates chemoresistance. J Transl Med. 2013;11:94.CrossRefPubMedPubMedCentral
85.
Tan AS, Baty JW, Dong LF, Bezawork-Geleta A, Endaya B, Goodwin J, et al. Mitochondrial genome acquisition restores respiratory function and tumorigenic potential of cancer cells without mitochondrial DNA. Cell Metab. 2015;21(1):81–94.CrossRefPubMed
86.
Shi LZ, Wang R, Huang G, Vogel P, Neale G, Green DR, et al. HIF1alpha-dependent glycolytic pathway orchestrates a metabolic checkpoint for the differentiation of TH17 and Treg cells. J Exp Med. 2011;208(7):1367–76.CrossRefPubMedPubMedCentral
87.
Wang T, Liu G, Wang R. The intercellular metabolic interplay between tumor and immune cells. Front Immunol. 2014;5:358.PubMedPubMedCentral
88.
89.
Ostuni R, Kratochvill F, Murray PJ, Natoli G. Macrophages and cancer: from mechanisms to therapeutic implications. Trends Immunol. 2015;36(4):229–39.CrossRefPubMed
90.
Al-Zoughbi W, Huang J, Paramasivan GS, Till H, Pichler M, Guertl-Lackner B, et al. Tumor macroenvironment and metabolism. Semin Oncol. 2014;41(2):281–95.CrossRefPubMed
91.
Mauer J, Denson JL, Bruning JC. Versatile functions for IL-6 in metabolism and cancer. Trends Immunol. 2015;36(2):92–101.CrossRefPubMed
92.
Martinez-Outschoorn UE, Whitaker-Menezes D, Lin Z, Flomenberg N, Howell A, Pestell RG, et al. Cytokine production and inflammation drive autophagy in the tumor microenvironment: role of stromal caveolin-1 as a key regulator. Cell Cycle. 2011;10(11):1784–93.CrossRefPubMedPubMedCentral
93.
Li D, Fu Z, Chen R, Zhao X, Zhou Y, Zeng B, et al. Inhibition of glutamine metabolism counteracts pancreatic cancer stem cell features and sensitizes cells to radiotherapy. Oncotarget. 2015;6(31):31151–63.PubMedPubMedCentral
94.
Wu Z, Wei D, Gao W, Xu Y, Hu Z, Ma Z, et al. TPO-induced metabolic reprogramming drives liver metastasis of colorectal cancer CD110+ tumor-initiating cells. Cell Stem Cell. 2015;17(1):47–59.CrossRefPubMed
95.
Ginestier C, Monville F, Wicinski J, Cabaud O, Cervera N, Josselin E, et al. Mevalonate metabolism regulates basal breast cancer stem cells and is a potential therapeutic target. Stem Cells. 2012;30(7):1327–37.CrossRefPubMed
96.
Ojha R, Bhattacharyya S, Singh SK. Autophagy in cancer stem cells: a potential link between chemoresistance, recurrence, and metastasis. Biores Open Access. 2015;4(1):97–108.CrossRefPubMedPubMedCentral
Metadata
Title
Cancer stem cell metabolism
Authors
Maria Peiris-Pagès
Ubaldo E. Martinez-Outschoorn
Richard G. Pestell
Federica Sotgia
Michael P. Lisanti
Publication date
01-12-2016
Publisher
BioMed Central
Published in
Breast Cancer Research / Issue 1/2016
Electronic ISSN: 1465-542X
DOI
https://doi.org/10.1186/s13058-016-0712-6

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