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转换Akt:从生存信号传导到致命反应。

Switching Akt: from survival signaling to deadly response.

作者信息

Los Marek, Maddika Subbareddy, Erb Bettina, Schulze-Osthoff Klaus

机构信息

Interfaculty Institute for Biochemistry, University of Tübingen, Tübingen, Germany.

出版信息

Bioessays. 2009 May;31(5):492-5. doi: 10.1002/bies.200900005.

Abstract

Akt, a protein kinase hyperactivated in many tumors, plays a major role in both cell survival and resistance to tumor therapy. A recent study,1 along with other evidences, shows interestingly, that Akt is not a single-function kinase, but may facilitate rather than inhibit cell death under certain conditions. This hitherto undetected function of Akt is accomplished by its ability to increase reactive oxygen species and to suppress antioxidant enzymes. The ability of Akt to down-regulate antioxidant defenses uncovers a novel Achilles' heel, which could be exploited by oxidant therapies in order to selectively eradicate tumor cells that express high levels of Akt activity.

摘要

Akt是一种在许多肿瘤中过度激活的蛋白激酶,在细胞存活和肿瘤治疗抗性方面都起着重要作用。最近的一项研究以及其他证据有趣地表明,Akt并非单一功能激酶,而是在某些条件下可能促进而非抑制细胞死亡。Akt这种迄今未被发现的功能是通过其增加活性氧物种和抑制抗氧化酶的能力来实现的。Akt下调抗氧化防御的能力揭示了一个新的致命弱点,氧化疗法可以利用这一点来选择性地根除表达高水平Akt活性的肿瘤细胞。

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