Blockage of PI3K/PKB/P27^(kip1) signaling pathway can antagonize 17β-estradiol-induced Ishikawa proliferation and cell cycle progression  

作　　者：GUO Rui-xia WEI Li-hui QIAO Yu-huan WANG Jian-liu TANG Jian-min 

机构地区：[1]Department of Gynecology, People＇s Hospital, Peking University,Beijing 100044, China [2]Department of Obstetrics and Gynecology, First Teaching Hospital,Zhengzhou University, Zhengzhou 450052, China [3]Department of Internal Medicine, People＇s Hospital, PekingUniversity, Beijing 100044, China

出　　处：《Chinese Medical Journal》2006年第3期242-245,共4页中华医学杂志（英文版）

基　　金：This study was partially supported by a grant from the Scientific Research Fund for Capital Medicine Development (No.ZD 199911).

摘　　要：It is well-known that risk for endometrial adenocarcinoma increases in patients with high level ofestrogen that is unopposed by progestin. And activation of extracellular signal-regulated kinase （ERK） and phosphatidylinositol 3 kinase/protein kinase B （PI3K/PKB） pathway are responsible for hormone-dependent cell growth in endometrial carcinoma. PI3K produces phosphatidylinositol- 3-phosphates by phosphory-lating the D3 hydroxyl of phosphoinositides, leading to membrane translocation of PKB,It is well-known that risk for endometrial adenocarcinoma increases in patients with high level ofestrogen that is unopposed by progestin. And activation of extracellular signal-regulated kinase （ERK） and phosphatidylinositol 3 kinase/protein kinase B （PI3K/PKB） pathway are responsible for hormone-dependent cell growth in endometrial carcinoma. PI3K produces phosphatidylinositol- 3-phosphates by phosphory-lating the D3 hydroxyl of phosphoinositides, leading to membrane translocation of PKB,

关 键 词：endometrial neoplasms ESTROGENS signal transduction pathway cell cycle cell proliferation 

分 类 号：R329.2[医药卫生—人体解剖和组织胚胎学]