Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is a tumor suppressor that is frequently down-modulated in human cancer. PTEN inhibits the phosphatidylinositol 3-phosphate kinase (PI3K)/AKT pathway through its lipid phosphatase activity. Multiple PI3K/AKT-independent actions of PTEN, protein-phosphatase activities and functions within the nucleus have also been described. PTEN, therefore, regulates many cellular processes including cell proliferation, survival, genomic integrity, polarity, migration, and invasion. Even a modest decrease in the functional dose of PTEN may promote cancer development. Understanding the molecular and cellular mechanisms that regulate PTEN protein levels and function, and how these may go awry in cancer contexts, is, therefore, key to fully understanding the role of PTEN in tumorigenesis. Here, we discuss current knowledge on posttranslational control and conformational plasticity of PTEN, as well as therapeutic possibilities toward reestablishment of PTEN tumor-suppressor activity in cancer.

中文翻译：

---

PTEN的翻译后调控和构象可塑性

在10号染色体（PTEN）上缺失的磷酸酶和张力蛋白同源物是一种抑癌基因，在人类癌症中常常被下调。PTEN通过其脂质磷酸酶活性来抑制磷脂酰肌醇3-磷酸激酶（PI3K）/ AKT途径。还描述了PTEN的多个不依赖PI3K / AKT的作用，蛋白磷酸酶活性和细胞核内的功能。因此，PTEN调节许多细胞过程，包括细胞增殖，存活，基因组完整性，极性，迁移和侵袭。即使PTEN功能剂量的适度降低也可能促进癌症的发展。因此，了解调节PTEN蛋白水平和功能的分子和细胞机制，以及在癌症情况下这些机制可能如何发挥作用，是全面了解PTEN在肿瘤发生中的作用的关键。这里，