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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >PTEN modulates cell cycle progression and cell survival by regulating phosphatidylinositol 3,4,5 ,-trisphosphate and Akt/protein kinase B signaling pathway
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PTEN modulates cell cycle progression and cell survival by regulating phosphatidylinositol 3,4,5 ,-trisphosphate and Akt/protein kinase B signaling pathway

机译：PTEN通过调节磷脂酰肌醇3,4,5，-三磷酸和Akt /蛋白激酶B信号通路来调节细胞周期进程和细胞存活

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摘要

To investigate the molecular basis of PTEN- mediated tumor suppression, we introduced a null mutation into the mouse Pten gene by homologous recombination in embryonic stem (ES) cells. Pten~-/- ES cells exhibited an increased growth rate and proliferated even in the absence of serum. ES cells lacking PTEN function also displayed advanced entry into S phase. This accelerated G_1/S transition was accompanied by down-regulation of p27~KIP1, a major inhibitor for G_1 cyclin- dependent kinases. Inactivation of PTEN in ES cells and in embryonic fibroblasts resulted in elevated levels of phosphati- dylinositol 3,4,5,-trisphosphate, a product of phosphatidylinosi- tol 3 kinase. Consequently, PTEN deficiency led to dosage- dependent increases in phosphorylation and activation of Akt/ protein kinase B, a well-characterized target of the phosphatidylinositol 3 kinase signaling pathway.Akt activation increased Bad phosphorylation and Promoted Pten~-/- cell sur- vival. Our studies suggest that PTEN regulates the phosphati- dylinositol 3,4,5,-trisphosphate and Akt signaling pathway and consequently modulates two critical cellular processes: cell cycle progression and cell survival.
机译：为了研究PTEN介导的肿瘤抑制的分子基础，我们通过胚胎干（ES）细胞中的同源重组将无效突变引入了小鼠Pten基因。即使在没有血清的情况下，Pten〜-/-ES细胞也表现出增加的生长速率并增殖。缺乏PTEN功能的ES细胞也显示出进入S期的高级状态。 G_1 / S的这种加速转变伴随着p27〜KIP1的下调，p27〜KIP1是G_1细胞周期蛋白依赖性激酶的主要抑制剂。 ES细胞和胚胎成纤维细胞中PTEN的失活导致磷脂酰肌醇3，4，5，-三磷酸，磷脂酰肌醇3激酶的产物，水平升高。因此，PTEN缺乏导致磷酸化和Akt /蛋白激酶B（磷脂酰肌醇3激酶信号转导通路的一个靶点）的剂量依赖性增加。Akt激活增加了不良的磷酸化并促进了Pten-/-细胞的存活。 。我们的研究表明，PTEN调节磷脂酰肌醇3,4,5，-三磷酸和Akt信号通路，从而调节两个关键的细胞过程：细胞周期进程和细胞存活。

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