Ginn-Pease Margaret E, Eng Charis
Clinical Cancer Genetics Program, Comprehensive Cancer Center, Columbus, Ohio 43210, USA.
Cancer Res. 2003 Jan 15;63(2):282-6.
Phosphatase and tensin homologue deleted on chromosome 10 (PTEN) is a tumor suppressor that causes cell cycle arrest. Lack of a nuclear locator sequence and a function in the cytosolic phosphatidylinositol 3'-kinase/Akt pathway diverted its study from the nucleus. However, immunohistochemistry revealed PTEN in the nucleus of normal cells and decreased nuclear PTEN in neoplastic tissues. Using protein expression analysis and fluoroscopic localization of green fluorescence protein-tagged PTEN, we examined nuclear PTEN in MCF-7 cells. We demonstrate that PTEN enters the nucleus and that nuclear PTEN varies throughout the cell cycle. Higher nuclear PTEN levels were associated with G0-G1 phase, and lower nuclear PTEN levels were associated with S phase. We postulate that nuclear PTEN activity might directly regulate the cell cycle.
10号染色体缺失的磷酸酶和张力蛋白同源物（PTEN）是一种导致细胞周期停滞的肿瘤抑制因子。由于缺乏核定位序列且在细胞质磷脂酰肌醇3'-激酶/蛋白激酶B（Akt）途径中发挥作用，其研究重点从细胞核转移。然而，免疫组织化学显示正常细胞的细胞核中有PTEN，而肿瘤组织中核PTEN减少。我们利用蛋白质表达分析和绿色荧光蛋白标记的PTEN的荧光定位，检测了MCF-7细胞中的核PTEN。我们证明PTEN进入细胞核，并且核PTEN在整个细胞周期中有所变化。较高的核PTEN水平与G0-G1期相关，而较低的核PTEN水平与S期相关。我们推测核PTEN活性可能直接调节细胞周期。
