Modulation of MnSOD in Cancer:Epidemiological and Experimental Evidence.
Modulation of MnSOD in Cancer:Epidemiological and Experimental Evidence.
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DOI：
10.5487/tr.2010.26.2.083
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发表时间：
2010-06
影响因子：
2.3
通讯作者：
Kim A
中科院分区：
文献类型：
--
作者：
Kim A
自从20世纪70年代末首次观察到人类癌症通常具有降低的锰超氧化物歧化酶（MnSOD）蛋白表达和活性以来，已经进行了广泛的研究以验证MnSOD与癌症之间的关联。MnSOD作为一种主要的线粒体抗氧化酶的意义是毋庸置疑的;体外、体内和流行病学研究的结果是一致的。相反，关于MnSOD在癌症中的作用的研究经常报告相互矛盾的结果。虽然已经提出了假定的机制来解释MnSOD如何调节细胞增殖，这些机制并没有在流行病学研究中投降。这篇综述讨论了最近的流行病学和实验研究，探讨MnSOD和癌症之间的关联，并介绍了新兴的MnSOD作为线粒体氧化还原调节酶的假设，以及如何改变线粒体氧化还原可能会影响生理的正常以及癌细胞。
Since it was first observed in late 1970s that human cancers often had decreased manganese superoxide dismutase (MnSOD) protein expression and activity, extensive studies have been conducted to verify the association between MnSOD and cancer. Significance of MnSOD as a primary mitochondrial antioxidant enzyme is unquestionable; results from in vitro, in vivo and epidemiological studies are in harmony. On the contrary, studies regarding roles of MnSOD in cancer often report conflicting results. Although putative mechanisms have been proposed to explain how MnSOD regulates cellular proliferation, these mechanisms are not capitulated in epidemiological studies. This review discusses most recent epidemiological and experimental studies that examined the association between MnSOD and cancer, and describes emerging hypotheses of MnSOD as a mitochondrial redox regulatory enzyme and of how altered mitochondrial redox may affect physiology of normal as well as cancer cells.