Cancer Genetics Program, Beth Israel Deaconess Cancer Center, Department of Medicine and Pathology, Harvard Medical School, Boston, Massachuchetts 02215, USA.
Nat Rev Mol Cell Biol. 2012 Apr 4;13(5):283-96. doi: 10.1038/nrm3330.
The importance of the physiological function of phosphatase and tensin homologue (PTEN) is illustrated by its frequent disruption in cancer. By suppressing the phosphoinositide 3-kinase (PI3K)-AKT-mammalian target of rapamycin (mTOR) pathway through its lipid phosphatase activity, PTEN governs a plethora of cellular processes including survival, proliferation, energy metabolism and cellular architecture. Consequently, mechanisms regulating PTEN expression and function, including transcriptional regulation, post-transcriptional regulation by non-coding RNAs, post-translational modifications and protein-protein interactions, are all altered in cancer. The repertoire of PTEN functions has recently been expanded to include phosphatase-independent activities and crucial functions within the nucleus. Our increasing knowledge of PTEN and pathologies in which its function is altered will undoubtedly inform the rational design of novel therapies.
磷酸酶和张力蛋白同源物（PTEN）的生理功能非常重要，其在癌症中经常发生缺失或失活。PTEN 通过其脂质磷酸酶活性抑制磷酸肌醇 3-激酶（PI3K）-蛋白激酶 B（AKT）-雷帕霉素哺乳动物靶蛋白（mTOR）通路，从而调控包括细胞存活、增殖、能量代谢和细胞结构在内的多种细胞过程。因此，调节 PTEN 表达和功能的机制，包括转录调控、非编码 RNA 的转录后调控、翻译后修饰和蛋白质-蛋白质相互作用，在癌症中均发生改变。PTEN 的功能组合最近已扩展到包括非依赖磷酸酶的活性以及在核内的关键功能。我们对 PTEN 及其功能改变相关疾病的认识不断加深，无疑将为新型治疗方法的合理设计提供信息。
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