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首页> 外文期刊>Journal of Cellular Physiology >Regulation of angiogenesis and tumor growth by p110 alpha and AKT1 via VEGF expression.
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Regulation of angiogenesis and tumor growth by p110 alpha and AKT1 via VEGF expression.

机译：监管的血管生成和肿瘤生长p110α和AKT1通过VEGF表达。

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Recent studies demonstrate that PI3K activation and PTEN mutation are frequently found in many human cancer cells and tissues. However, the mechanism of PI3K signaling in human cancer tumorigenesis remains to be elucidated. In this study we specifically downregulated p110alpha expression in ovarian cancer cells using siRNA interference. We found that p110alpha downregulation greatly decreased ovarian tumor growth and angiogenesis, and that p110alpha siRNA inhibited VEGF expression through decreasing hypoxia-inducible factor 1alpha expression in both ovarian cancer cells and tumor tissues. To determine the downstream targets of PI3K in regulating tumor growth and angiogenesis, we find that AKT1 is a major downstream mediator for regulating tumor growth, angiogenesis, and VEGF expression. These data show that p110alpha and AKT1 play an important role in tumor growth by inducing angiogenesis and by increasing HIF-1alpha and VEGF expression. This work provides a better understanding of the molecular mechanism of human cancer induced by the activation of PI3K signaling.
机译：最近的研究表明,PI3K激活和PTEN突变是经常发现在许多人类癌症细胞和组织。PI3K信号机制在人类癌症肿瘤发生还有待阐明。研究中我们专门p110alpha使之抑制使用核的卵巢癌细胞中的表达干扰。downregulation大大减少卵巢肿瘤生长和血管生成,p110alpha核通过减少抑制VEGF的表达低氧诱导因子1α表达卵巢癌细胞和肿瘤组织。确定PI3K的下游目标调节肿瘤生长和血管生成,我们发现AKT1主要下游中介调节肿瘤生长、血管生成和VEGF表达式。AKT1发挥重要作用在肿瘤的生长诱导血管生成和增加HIF-1alpha和VEGF表达。提供了一个更好的理解的分子人类癌症诱导的机制激活PI3K信号。

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