抑制癌症中的线粒体重编程
Disabling mitochondrial reprogramming in cancer.
作者信息
Caino M Cecilia, Altieri Dario C
机构信息
Prostate Cancer Discovery and Development Program, Tumor Microenvironment and Metastasis Program, The Wistar Institute, Philadelphia, PA 19104, United States.
Prostate Cancer Discovery and Development Program, Tumor Microenvironment and Metastasis Program, The Wistar Institute, Philadelphia, PA 19104, United States.
出版信息
Pharmacol Res. 2015 Dec;102:42-5. doi: 10.1016/j.phrs.2015.08.022. Epub 2015 Sep 10.
Abstract
Recent studies have demonstrated that tumor cells exposed to molecular therapy with PI3K antagonists redistribute their mitochondria to the peripheral cytoskeleton, fueling membrane dynamics, turnover of focal adhesion complexes and increased tumor cell motility and invasion. Although this process paradoxically increases metastatic propensity during molecular therapy, it also emphasizes a critical role of regional mitochondrial bioenergetics in tumor metabolic reprogramming and may offer prime therapeutic opportunities to prevent disseminated disease.
摘要
最近的研究表明，暴露于PI3K拮抗剂分子疗法的肿瘤细胞会将其线粒体重新分布到外周细胞骨架，为膜动力学、粘着斑复合物的周转提供能量，并增加肿瘤细胞的运动性和侵袭性。尽管这一过程在分子治疗期间反常地增加了转移倾向，但它也强调了局部线粒体生物能量学在肿瘤代谢重编程中的关键作用，并可能提供预防播散性疾病的主要治疗机会。
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Mol Cell. 2015 Feb 5;57(3):521-36. doi: 10.1016/j.molcel.2015.01.003.
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