探讨miR-125b过表达对子宫内膜癌（endometrial carcinoma, EC）HEC-1B细胞增殖及凋亡的影响及其可能的机制。方法：收集2012年11月至2013年11月间四川省妇幼保健医院收治的30例子宫内膜样腺癌患者肿瘤及其癌旁组织标本，Real-time PCR检测肿瘤组织及培养细胞中miR-125b的表达水平。脂质体转染法分别将miR-125b模拟片段（mimic）与无关序列（scramble mimic）转染入HEC-1B细胞作为miR-125b组和对照组，以野生型HEC-1B细胞为未处理组。流式细胞术和CCK-8法分别检测过表达miR-125b对HEC-1B细胞周期、凋亡和增殖的影响，Western blotting检测过表达miR-125b对HEC-1B细胞中PIK3CD、p-AKT以及总AKT表达的影响。结果：人EC组织中miR-125b表达量较癌旁组织显著下调（P<005）。HEC-1B细胞转染mimic片段后，其miR-125b的表达上调820倍以上。转染48 h后，miR-125b组细胞的增殖能力显著低于对照组和未处理组（0.53±0.06 vs 0.82±0.07、0.89±0.08，P<0.01）、细胞凋亡率显著升高[（21.5±3.2）% vs （142±2.3）%、（13.5±2.1）%，均P＜0.01]，并且miR-125b组细胞周期阻滞于G1期；miR-125b组HEC-1B细胞中PIK3CD及其下游p-AKT蛋白表达较对照组和未处理组显著降低（均P<0.01），而总AKT表达无明显变化（均P＞0.05）。结论：miR-125b在EC组织中普遍低表达，其在HEC-1B细胞中过表达能够明显抑制细胞增殖和周期进程，促进细胞早期凋亡，这可能与miR-125过表达抑制细胞内PI3K/AKT信号通路有关。

To investigate the effects and underlying mechanisms of miR-125b overexpression on proliferation and apoptosis of endometrial carcinoma (EC) HEC-1B cells in vitro. Methods: Paired EC tissue and adjacent tissue specimens were collected from 30 patients with EC who were treated in the Department of Gynecology and Obstetrics, Sichuan Women’s and Children's Hospital between November 2012 and November 2013. Levels of miR-125b mRNA in these specimens were assessed by real-time PCR. To elucidate the effect and mechanisms of miR-125b overexpression on EC cell death/survival, HEC-1B cells were transfected with an expression vector containing a mimic fragment of miR-125b and a control vector with a sequenced-scrambled fragment, respectively, using lipofectamine were, and cell proliferation, cell cycle progression/apoptosis, and protein levels of PIK3CD, p-AKT and total Akt were assessed by cell counting kit-8 (CCK-8) assays, flow cytometery and Western blotting analysis, respectively, in the transfectants and wild type HEC-1B cells. Results: In all 30 paired specimens, miR-125b mRNA abundance was significantly lower in the endometrial cancer tissue than in the adjacent normal tissue (P<0.05). Transfection of HEC-1B cells with the miR-125b vector resulted in an increase in miR-125b mRNA by more than 820 times. The proliferation index was 0.53±0.06 in HEC-1B cells overexpressing miR-125b, significantly higher (P<0.05) than that in HEC-1B cells overexpressing the sequence-scrambled fragment (0.82±0.07) and wild-type HEC-1B cells (0.89±0.08). The rate of apoptosis with G1 phase arrest was significantly higher in miR-125b-transfected HEC-1B cells as compared with control vector-transfected and wild-type HEC-1B cells ([21.5±3.2]% vs [14.2±2.3]% and [13.5±2.1]%, P<0.01). While no significant difference was observed in total Akt protein content among the three groups of HEC-1B cells (P>0.05), protein contents of PIK3CD and p-AKT were significantly reduced in HEC-1B cells transfected with miR-125b compared with cells transfeced with the control vector and untreated HEC-1B cells (P<0.01). Conclusion: The expression of miR-125b is significantly decreased in the EC tissue. Overexpression of miR-125b may suppress cell proliferation and cell cycle progression and induce cell apoptosis , possibly through suppressing the PI3K/AKT signaling pathway, in HEC-B cells in vitro.