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利用线粒体凋亡治疗癌症。

Exploiting mitochondrial apoptosis for the treatment of cancer.

机构信息

Institute for Experimental Cancer Research in Pediatrics, Goethe-University Frankfurt, Germany.

出版信息

Mitochondrion. 2010 Nov;10(6):598-603. doi: 10.1016/j.mito.2010.05.001. Epub 2010 May 16.

Abstract

Mitochondria are key regulators of many forms of cell death and often altered in human malignancies. Since the inefficacy of established cancer therapies is, at least to a large extent, the result of oncogenic blockade of cell death pathways, compounds that directly affect mitochondrial functions are considered to present a promising alternative approach to eradicate chemotherapy-resistant cancer cells. Since mitochondria-targeted drugs can directly initiate mitochondrial perturbations independent of upstream signaling events, these agents may induce cell death and overcome drug resistance under circumstances, where conventional drugs fail to act because pathways upstream of mitochondria are frequently disrupted in cancer cells. A better understanding of the fundamental mechanisms that govern the complex processes of mitochondrial apoptosis is expected to open new perspectives for cancer drug development. Hopefully, this knowledge will eventually be translated into medical application for the treatment of human cancer.

摘要

线粒体是多种细胞死亡形式的关键调节剂,并且经常在人类恶性肿瘤中发生改变。由于既定癌症疗法的无效性至少在很大程度上是由于致癌性阻断细胞死亡途径的结果,因此直接影响线粒体功能的化合物被认为是一种有前途的替代方法,可以根除化疗耐药的癌细胞。由于线粒体靶向药物可以独立于上游信号事件直接引发线粒体扰动,因此这些药物可以在常规药物因线粒体上游途径经常在癌细胞中被破坏而无法发挥作用的情况下诱导细胞死亡并克服耐药性。更好地了解控制线粒体凋亡复杂过程的基本机制有望为癌症药物开发开辟新的视角。希望这些知识最终能够转化为治疗人类癌症的医学应用。

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