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PTEN and Tumor
Abstract. PTEN was the firstly found cancer suppressor gene with dual-specificity phosphatase (DPS) activities. The gene has connection with the sporadic tumors and hereditary diseases characterized by tumor-like growth in humans. PTEN can specifically dephosphorylate the phosphatidylinositol-3, 4, 5-triphosphoric acid [PIP3], and antagonize PI3K-AKT signaling pathway to be at work, and hence regulates the growth, multiplication, migration and apoptosis of cells. PTEN mutations are mainly reflected in genic mutation and heterozygous losses, which is involved in the occurrance, development and prognosis of multiple tumors.
Key words: cancer suppressor gene, PTEN, tumor, phosphatase
1. Introduction
The occurrance, development, invasion and metastasis of tumor are processes of changes in multiple factors, steps and genes, in which the activation of cancer genes and the inactivation of cancer suppressor genes are important factors. Li et al [1] (1997) cloned a new gene when researching the primary breast cancer 10q23 homology loss region and named it phosphatase and tensin homology deleted on chromosome 10 (PTEN). In the same year, Steck et al [2] cloned a tumor suppressor gene in 10q23。3 in the research of glioblastoma multiforme cell line and named it Mutated in Multiple Advanced Cancers (MMAC). Li et al [3] found the epithelial cell regulated by GF-βwas rich in phosphatase 1 (TEP1). These three genes are identified as a same cancer suppressor gene with dual-specificity phosphatase activities; the mutation and deletion of this gene has connection with multiple tumors in humans. The existing researches have confirmed the mutation and deletion of this gene in glioblastoma, prostate cancer, breast cancer, endometrial cancer, liver cancer, gastric cancer, carcinoma of the rectum, esophageal cancer, lung cancer, transitional cell carcinoma of bladder, and even mouth neoplasm, hematological cancer, etc. [1-4]
2. Molecular Structure and Biol
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