目的 探讨人子宫内膜癌细胞Ishikawa和RL95-2中SOS-Ras/Rac鸟嘌呤核苷酸交换因子1-内含子转录物1（SOS1-IT1）影响zeste同源物增强子2（EZH2）蛋白表达的分子机制。方法在Ishikawa和RL95-2细胞系中利用慢病毒转染短发夹RNA（shRNA）和过表达质粒方法，敲低和过表达SOS1-IT1，利用Real-time PCR、Western blotting和染色质免疫共沉淀等实验探究EZH2表达调控的机制。结果  SOS1-IT1与EZH2基因在人子宫内膜癌组织中的表达成正相关，敲低SOS1-IT1明显降低EZH2的表达，抑制Ishikawa和RL95-2细胞增殖和迁移，且能降低EZH2基因启动区组蛋白H3第27位点的赖氨酸（H3K27）乙酰化和CREB结合蛋白（CBP）的富集程度，而过表达SOS1-IT1则可以增加EZH2的表达量，并增强H3K27乙酰化和CBP的富集程度，且CBP可以结合SOS1-IT1 RNA，在敲低CBP时，这种结合能力减弱。结论  SOS1-IT1可以通过调控EZH2基因启动子区的乙酰化修饰水平促进子宫内膜癌细胞Ishikawa和RL95-2中EZH2的表达水平，进而影响子宫内膜癌细胞的增殖和迁移能力。

Objective To explore the molecular mechanism by which SOS Ras/Rac guanine nucleotide exchange factor 1-intronic transcript 1 (SOS1-IT1) affects enhancer of zeste homolog 2 (EZH2) protein expression in endometrial cancer cells Ishikawa and RL95-2.   Methods  Lentiviral transfection of short hairpin RNA(shRNA) and overexpression plasmid were used in Ishikawa and RL95-2 cell lines to knock down and overexpress SOS1-IT1. The mechanism of EZH2 expression regulation was studied using Real-time PCR, Western blotting, and chromatin immunoprecipitation.  Results The expression of SOS1-IT1 and EZH2 genes was positively correlated in endometrial cancer tissues. Knocking down SOS1-IT1 significantly reduces the expression of EZH2, inhibited the proliferation and migration of Ishikawa and RL95-2 cells, and could reduced the acetylation of histone H3 at position 27 (H3K27) and the enrichment of CREB binding protein (CBP) in the EZH2 gene promoter region. Overexpression of SOS1-IT1 could increased the expression of EZH2 and enhance the acetylation of H3K27 and the enrichment of CBP. CBP could bind to SOS1-IT1 RNA, and this binding ability was weakened when CBP was knocked down. Conclusion   SOS1-IT1 can promote the expression level of EZH2 in endometrial cancer cells Ishikawa and RL95-2 by regulating the acetylation modification level of the EZH2 gene promoter region, thereby affecting the proliferation and migration ability of endometrial cancer cells.