Metabolic hijacking: A survival strategy cancer cells exploit?

被引:26
作者
Mitchell, Megan I. [1 ]
Engelbrecht, Anna-Mart [1 ]
机构
[1] Univ Stellenbosch, Dept Physiol Sci, Merriman Rd & Bosman Rd,Mike Vries Bldg, ZA-7602 Stellenbosch, South Africa
基金
新加坡国家研究基金会; 英国医学研究理事会;
关键词
Cancer-associated fibroblasts; Chemoresistance; Cell death; Reverse "Warburg" effect; FORKHEAD TRANSCRIPTION FACTORS; ORAL SODIUM PHENYLBUTYRATE; CHEMOKINE RECEPTOR CXCR4; BREAST-CANCER; OXIDATIVE STRESS; MITOCHONDRIAL DYSFUNCTION; TUMOR PROGRESSION; DOSE-ESCALATION; STEM-CELLS; TGF-BETA;
D O I
10.1016/j.critrevonc.2016.11.010
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The majority of human tumours are comprised of cancerous epithelial cells that coexist with a multitude of different cell types and extracellular matrix components creating the cancer microenvironment. Cancer-associated fibroblasts (CAFs) are the most abundant mesenchymal cell types present within most human carcinomas. Recent evidence suggests that nutrient deprived epithelial cancer cells are able to survive these conditions, as a result of their ability to undergo extensive metabolic reprogramming and exploit the metabolic capacities of surrounding CAFs. Although several studies support the role of CAFs in tumour progression and metastasis, the molecular mechanisms underlying this pro-tumourigenic interaction remains to be elucidated. This review will discuss the complex metabolic interaction that exists between epithelial cancer cells and CAF's: focussing primarily on their functional role in tumour progression, metastasis and chemotherapeutic resistance. Attempts are made at delineating the molecular mechanisms underlying this pro-tumourigenic interaction, and potential CAF-based targets are suggested. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:1 / 8
页数:8
相关论文
共 80 条
[1]  
[Anonymous], 2014, PLOS ONE
[2]   Expert opinion on the use of anthracyclines in patients with advanced breast cancer at cardiac risk [J].
Barrett-Lee, P. J. ;
Dixon, J. M. ;
Farrell, C. ;
Jones, A. ;
Leonard, R. ;
Murray, N. ;
Palmieri, C. ;
Plummer, C. J. ;
Stanley, A. ;
Verrill, M. W. .
ANNALS OF ONCOLOGY, 2009, 20 (05) :816-827
[3]   Activation of the integrins α5β1 and αvβ3 and focal adhesion kinase (FAK) during arteriogenesis [J].
Cai, Wei-Jun ;
Li, Ming Bo ;
Wu, Xiaoqiong ;
Wu, Song ;
Zhu, Wu ;
Chen, Dan ;
Luo, Mingying ;
Eitenmueller, Inka ;
Kampmann, Andreas ;
Schaper, Jutta ;
Schaper, Wolfgang .
MOLECULAR AND CELLULAR BIOCHEMISTRY, 2009, 322 (1-2) :161-169
[4]   Integrin Structure, Activation, and Interactions [J].
Campbell, Iain D. ;
Humphries, Martin J. .
COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY, 2011, 3 (03) :1-14
[5]  
Capparelli C., 2011, ABBV CELL CYCLE, V11, P2285
[6]   Metabolism and epigenetics: a link cancer cells exploit [J].
Carrer, Alessandro ;
Wellen, Kathryn E. .
CURRENT OPINION IN BIOTECHNOLOGY, 2015, 34 :23-29
[7]   Oxidative stress induces autophagic cell death independent of apoptosis in transformed and cancer cells [J].
Chen, Y. ;
McMillan-Ward, E. ;
Kong, J. ;
Israels, S. J. ;
Gibson, S. B. .
CELL DEATH AND DIFFERENTIATION, 2008, 15 (01) :171-182
[8]   Potential role of HER2-overexpressing exosomes in countering trastuzumab-based therapy [J].
Ciravolo, Valentina ;
Huber, Veronica ;
Ghedini, Gaia C. ;
Venturelli, Elisabetta ;
Bianchi, Francesca ;
Campiglio, Manuela ;
Morelli, Daniele ;
Villa, Antonello ;
Della Mina, Pamela ;
Menard, Sylvie ;
Filipazzi, Paola ;
Rivoltini, Licia ;
Tagliabue, Elda ;
Pupa, Serenella M. .
JOURNAL OF CELLULAR PHYSIOLOGY, 2012, 227 (02) :658-667
[9]   Mechanisms and strategies to overcome chemotherapy resistance in metastatic breast cancer [J].
Coley, Helen M. .
CANCER TREATMENT REVIEWS, 2008, 34 (04) :378-390
[10]   Akt phosphorylation of BAD couples survival signals to the cell-intrinsic death machinery [J].
Datta, SR ;
Dudek, H ;
Tao, X ;
Masters, S ;
Fu, HA ;
Gotoh, Y ;
Greenberg, ME .
CELL, 1997, 91 (02) :231-241