中文摘要：

背景类型我释放 gonadotropin 荷尔蒙(GnRH-l ) 收缩筋被申请了象胸癌，卵巢的癌症和 prostatic 癌那样的类固醇依赖者肿瘤的治疗。但是机制还没被澄清。关于用 GnRH-l 收缩筋的子宫内膜的癌的治疗有很少报告。类型 II GnRH (GnRH-ll ) 是 GnRH 的一种新子类型。我们的目的是在雌激素上调查 GnRH-l 收缩筋和 GnRH-ll 的效果受体否定的从到 them.Methods 的磷酸酶和 tensin 相当或相同的事物基因(PTEN ) 的人的子宫内膜的癌房间和效果 lentiviral 调停向量的 RNAi 方法被用来建立 PTEN 否定的 HEC-1A 房间克隆(HEC-1A-ND ) 。MTT 和流动 cytometry 被用来与 GnRH-l 收缩筋 Triptorelin (到 10-5 mol/L 的 10-11 mol/L ) 或 GnRH-ll (到 10-5 mol/L 的 10-11 mol/L ) 在治疗以后检测房间增长，房间周期和 HEC-1A， HEC-1A-NC 和 HEC-1A-ND 房间的 apoptosis。西方的弄污被用来与 Triptorelin 的不同集中在治疗以后检测 AKT 和 ERK1/2 激活或为 30 的 GnRH-ll 在提及的上面纪录三种房间。结果 Triptorelin 和 GnRH-ll 导致了 apoptosis 并且以一种剂量依赖者方式禁止了 HEC-1 A， HEC-1A-ND 和 HEC-1A-NC 的增长。这效果在 PTEN 基因在是组合式的 HEC-1 和房间被扩充。而且， Triptorelin 和 GnRH-ll 在 HEC-1 和 cells.Conclusions Triptorelin 和 GnRH-ll 禁止了 AKT 和英皇家空军之阶级最低之兵活动能支持 apoptosis 率并且禁止雌激素的房间增长以一种剂量依赖者方式的受体否定的子宫内膜的癌房间。PTEN 基因能在人的子宫内膜的癌房间上禁止 Triptorelin 或 GnRH-ll 的效果。

英文摘要：

Background Type I gonadotropin-releasing hormone （GnRH-l） agonists have been applied for the treatment of steroid-dependent tumors such as breast carcinoma, ovarian cancer and prostatic carcinoma. But the mechanism has not been clarified yet. There are few reports about the treatment of endometrial carcinoma using GnRH-l agonists. Type II GnRH （GnRH-ll） is a new subtype of GnRH. Our aim was to investigate the effects of GnRH-l agonists and GnRH-ll on estrogen receptor-negative human endometrial carcinoma cells and the effect from phosphatase and tensin homolog gene （PTEN） to them.Methods A lentiviral vector-mediated RNAi method was used to establish a PTEN-negative HEC-1A cell clone （HEC-1A-ND）. MTT and flow cytometry were used to detect the cell proliferation, cell cycle and apoptosis of HEC-1A, HEC-1A-NC and HEC-1A-ND cells after treatment with GnRH-l agonist Triptorelin （10-11 mol/L to 10-5 mol/L） or GnRH-ll （10-11 mol/L to 10-5 mol/L）. Western blotting was used to detect AKT and ERK1/2 activation after treatment with different concentrations of Triptorelin or GnRH-ll for 30 minutes in the above mentioned three kinds of cells. Results Triptorelin and GnRH-ll induced apoptosis and inhibited proliferation of HEC-1 A, HEC-1A-ND and HEC-1A-NC in a dose-dependent manner. This effect was augmented in HEC-1 A-ND cells in which PTEN gene was knocked-down. Furthermore, Triptorelin and GnRH-ll inhibited the AKT and ERK activity in HEC-1 A-ND cells.Conclusions Triptorelin and GnRH-ll can promote apoptosis rate and inhibit cell proliferation of estrogen receptor-negative endometrial carcinoma cells in a dose-dependent manner. PTEN gene can inhibit the effects of Triptorelin or GnRH-ll on human endometrial carcinoma cells.