Mitochondrial biology in cancer stem cells

被引:37
|
作者
Loureiro, Rute [1 ]
Mesquita, Katia A. [2 ]
Magalhaes-Novais, Silvia [2 ]
Oliveira, Paulo J. [2 ]
Vega-Naredo, Ignacio [2 ,3 ]
机构
[1] Max Planck Inst Metab Res, D-50931 Cologne, Germany
[2] Univ Coimbra, CNC Ctr Neurosci & Cell Biol, UC Biotech Bldg,Biocant Pk, P-3060197 Cantanhede, Portugal
[3] Univ Oviedo, Dept Morphol & Cell Biol, E-33006 Oviedo, Spain
关键词
Mitochondria; Cancer stem cells; Metabolism; Chemotherapy; Cell death; FATTY-ACID OXIDATION; OXYGEN SPECIES GENERATION; INDUCIBLE FACTOR 1-ALPHA; ACUTE MYELOID-LEUKEMIA; BREAST-CANCER; TUMOR-GROWTH; PERMEABILITY TRANSITION; SIDE-POPULATION; PHARMACOLOGICAL INHIBITION; PROSPECTIVE IDENTIFICATION;
D O I
10.1016/j.semcancer.2017.06.012
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Cancer stem cells (CSCs) have been suggested to be responsible for tumor re-growth and relapse. Physiological and morphological knowledge of CSCs may be essential for the development of new therapeutic strategies targeting cancer development, progression, and recurrence. Current research is focused on a deeper understanding of CSCs metabolic profiles, taking into consideration their energy demands. Energy metabolism and mitochondrial function are important factors operating on sternness maintenance and cell fate specification. Due to the role of mitochondria as central hubs in the overall cell metabolism and death and survival pathways, research on their physiology in CSCs is of paramount importance to decipher mechanisms underlying their therapy-resistant phenotype. In this review, we focus on CSCs mitochondrial biology and mitochondria-related signaling pathways that contribute to CSCs survival and maintenance, thereby representing possible therapeutic targets.
引用
收藏
页码:18 / 28
页数:11
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