作者: D.-M. Li , H. Sun
关键词:
摘要: PTEN/MMAC1/TEP1 is a tumor suppressor that possesses intrinsic phosphatase activity. Deletions or mutations of its encoding gene are associated with variety human cancers. However, very little known about the molecular mechanisms by which this important regulates cell growth. Here, we show PTEN expression potently suppressed growth and tumorigenicity glioblastoma U87MG cells. The suppression activity was mediated ability to block cycle progression in G1 phase. Such an arrest correlated significant increase kinase inhibitor p27KIP1 concomitant decrease activities cyclin-dependent kinases. also led inhibition Akt/protein B, serine-threonine activated phosphatidylinositol 3-kinase (PI 3-kinase) signaling pathway. In addition, effect on can be mimicked treatment cells LY294002, selective PI 3-kinase. Taken together, our studies suggest modulates through negatively regulating 3-kinase/Akt pathway, one critical target process p27KIP1.