Instituto de Biomedicina de Sevilla (IBIS), Hospital Universitario Virgen del Rocío, Universidad de Sevilla, Consejo Superior de Investigaciones Científicas, Avda. Manuel Siurot s/n, 41013 Seville, Spain.
Departamento de Bioquímica Vegetal y Biología Molecular, Universidad de Sevilla, Facultad de Biología, Avda. de la Reina Mercedes 6, 41012 Seville, Spain.
Cells. 2020 Jul 15;9(7):1693. doi: 10.3390/cells9071693.
Cancer stem cells (CSC) are associated with the mechanisms of chemoresistance to different cytotoxic drugs or radiotherapy, as well as with tumor relapse and a poor prognosis. Various studies have shown that mitochondria play a central role in these processes because of the ability of this organelle to modify cell metabolism, allowing survival and avoiding apoptosis clearance of cancer cells. Thus, the whole mitochondrial cycle, from its biogenesis to its death, either by mitophagy or by apoptosis, can be targeted by different drugs to reduce mitochondrial fitness, allowing for a restored or increased sensitivity to chemotherapeutic drugs. Once mitochondrial misbalance is induced by a specific drug in any of the processes of mitochondrial metabolism, two elements are commonly boosted: an increment in reactive nitrogen/oxygen species and, subsequently, activation of the intrinsic apoptotic pathway.
肿瘤干细胞（CSC）与不同细胞毒性药物或放射疗法的化疗耐药机制、肿瘤复发和预后不良有关。多项研究表明，由于线粒体能够改变细胞代谢，使癌细胞存活并避免细胞凋亡清除，因此在这些过程中线粒体起着核心作用。因此，整个线粒体周期，从生物发生到死亡，无论是通过自噬还是通过细胞凋亡，都可以被不同的药物靶向，以降低线粒体适应性，从而使癌细胞对化疗药物的敏感性恢复或增加。一旦线粒体代谢的任何过程中特定药物引起线粒体失衡，通常会增强两个因素：活性氮/氧物种的增加，随后内在凋亡途径的激活。
