The PTEN/MMAC1 tumor suppressor induces cell death that is rescued by the AKT/protein kinase B oncogene.
The PTEN/MMAC1 tumor suppressor induces cell death that is rescued by the AKT/protein kinase B oncogene.
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发表时间：
1998-12
期刊：
影响因子：
11.2
通讯作者：
Jing Li;Jing Li;Laura Simpson;Laura Simpson;M. Takahashi;M. Takahashi;C. Miliaresis;C. Miliaresis
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文献类型：
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作者：
Jing Li;Jing Li;Laura Simpson;Laura Simpson;M. Takahashi;M. Takahashi;C. Miliaresis;C. Miliaresis
PTEN/MMAC1 是一种肿瘤抑制基因，在多种癌症中发生突变。 PTEN 编码一种磷酸酶，可识别磷蛋白底物和磷脂（3,4,5-三磷酸磷脂酰肌醇）。 PTEN 抑制所有测试的上皮细胞系中的细胞生长和/或集落形成，只有一种例外。细胞增殖的减少与细胞凋亡的诱导和通过磷脂酰肌醇3'-激酶途径的信号传导的抑制有关。 Akt/蛋白激酶 B 是一种抗凋亡功能受 3,4,5-三磷酸磷脂酰肌醇调节的基因，能够将细胞从 PTEN 依赖性死亡中拯救出来。因此，PTEN 似乎通过调节磷脂酰肌醇 3'-激酶信号传导来抑制肿瘤生长。
PTEN/MMAC1 is a tumor suppressor gene that is mutated in a variety of cancers. PTEN encodes a phosphatase that recognizes phosphoprotein substrates and the phospholipid, phosphatidylinositol-3,4,5-triphosphate. PTEN inhibited cell growth and/or colony formation in all of the epithelial lines tested with one exception. The decrease in cellular proliferation was associated with an induction of apoptosis and an inhibition of signaling through the phosphatidylinositol 3'-kinase pathway. Akt/protein kinase B, a gene whose antiapoptotic function is regulated by phosphatidylinositol-3,4,5-triphosphate, was able to rescue cells from PTEN-dependent death. PTEN, therefore, appears to suppress tumor growth by regulating phosphatidylinositol 3'-kinase signaling.