PTEN公司
张力素
磷酸酶
鸟嘌呤核苷酸交换因子
PI3K/AKT/mTOR通路
癌症研究
信号转导
抑癌基因
化学
蛋白激酶B
细胞生物学
生物
磷酸化
生物化学
基因
癌变
作者
Barry Fine,Cindy Hodakoski,Susan Koujak,Tao Su,Lao H. Saal,Matthew Maurer,Benjamin D. Hopkins,Megan Keniry,Maria Luisa Sulis,Sarah M. Mense,Hanina Hibshoosh,Ramon Parsons
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:2009-09-04
卷期号:325 (5945): 1261-1265
被引量:210
标识
DOI:10.1126/science.1173569
摘要
PTEN (phosphatase and tensin homolog on chromosome 10) is a tumor suppressor whose cellular regulation remains incompletely understood. We identified phosphatidylinositol 3,4,5-trisphosphate RAC exchanger 2a (P-REX2a) as a PTEN-interacting protein. P-REX2a mRNA was more abundant in human cancer cells and significantly increased in tumors with wild-type PTEN that expressed an activated mutant of PIK3CA encoding the p110 subunit of phosphoinositide 3-kinase subunit alpha (PI3Kalpha). P-REX2a inhibited PTEN lipid phosphatase activity and stimulated the PI3K pathway only in the presence of PTEN. P-REX2a stimulated cell growth and cooperated with a PIK3CA mutant to promote growth factor-independent proliferation and transformation. Depletion of P-REX2a reduced amounts of phosphorylated AKT and growth in human cell lines with intact PTEN. Thus, P-REX2a is a component of the PI3K pathway that can antagonize PTEN in cancer cells.
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