Simpson L, Parsons R
Institute of Cancer Genetics, College of Physicians and Surgeons, Columbia University, 1150 St. Nicholas Avenue, Russ Berrie Pavilion Room 302, New York, New York 10032, USA.
Exp Cell Res. 2001 Mar 10;264(1):29-41. doi: 10.1006/excr.2000.5130.
PTEN, a tumor suppressor located at chromosome 10q23, is mutated in a variety of sporadic cancers and in two autosomal dominant hamartoma syndromes. PTEN is a phosphatase which dephosphorylates phosphatidylinositol (3,4,5)-triphosphate (PtdIns-3,4,5-P3), an important intracellular second messenger, lowering its level within the cell. By dephosphorylating PtdIns-3,4,5-P3, PTEN acts in opposition to phosphatidylinositol 3-kinase (PI3K), which has a pivotal role in the creation of PtdIns-3,4,5-P3. PtdIns-3,4,5-P3 is necessary for the activation of Akt, a serine/threonine kinase involved in cell growth and survival. By blocking the activation of Akt, PTEN regulates cellular processes such as cell cycling, translation, and apoptosis. In this review, we will discuss the identification of PTEN, its mutational status in cancer, its role as a regulator of PI3K, and its domain structure.
PTEN是一种位于10号染色体q23区域的肿瘤抑制基因，在多种散发性癌症以及两种常染色体显性错构瘤综合征中发生突变。PTEN是一种磷酸酶，可使磷脂酰肌醇（3,4,5）-三磷酸（PtdIns-3,4,5-P3）去磷酸化，PtdIns-3,4,5-P3是一种重要的细胞内第二信使，可降低其在细胞内的水平。通过使PtdIns-3,4,5-P3去磷酸化，PTEN的作用与磷脂酰肌醇3激酶（PI3K）相反，PI3K在PtdIns-3,4,5-P3的生成中起关键作用。PtdIns-3,4,5-P3是激活Akt所必需的，Akt是一种参与细胞生长和存活的丝氨酸/苏氨酸激酶。通过阻断Akt的激活，PTEN调节细胞周期、翻译和凋亡等细胞过程。在本综述中，我们将讨论PTEN的鉴定、其在癌症中的突变状态、其作为PI3K调节剂的作用及其结构域结构。
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