人类子宫内膜在月经周期中经历了剧烈的改建，这对于成功的囊胚附着和着床在中期分泌（可接受）阶段至关重要。microRNA（miR）在子宫内膜接受性准备中发挥作用。miR-23b-3p的表达在可生育子宫内膜期间增加。本研究旨在调查miR-23b-3p在子宫内膜接受性期间的功能。利用qPCR和原位杂交技术分别研究miR-23b-3p在人类子宫内膜中的表达和定位。接种miR-23b-3p模拟物的Ishikawa细胞（子宫内膜上皮细胞系）和来自子宫内膜器官的上皮细胞进行克隆，并使用滋养细胞前体球（囊胚替代物）粘附试验来确定其对囊胚粘附于子宫内膜细胞上的影响。我们证明，与不可接受的增生期相比，接受期内生育子宫内膜中的miR-23b-3p显著上调。在可生育和不孕的中期分泌期子宫内膜中，miR-23b-3p的表达没有差异。miR-23b-3p在中期分泌期上皮和基质中有定位，但在可生育子宫内膜的增生期中无法检测到。从功能上讲，Ishikawa细胞和可生育子宫内膜器官源性上皮细胞中miR-23-3p的过度表达显著改善了它们与滋养细胞前体球的粘附能力。在不孕的子宫内膜器官源性上皮细胞中过度表达miR-23b-3p无法改善粘附。在检查的10个miR预测基因靶点中，与对照相比，Ishikawa细胞中miR-23b-3p的过度表达显著降低了MET、SFRP4和ACADSB的表达。在可生育器官源性上皮细胞中，过度表达miR23b-3p后SFRP4的降解通过免疫印迹得到证实。可生育子宫内膜中的SFRP4表达呈相反的表达模式，与miR-23b-3p相比，在增生期高于中期分泌期。总的来说，miR-23b-3p很可能是子宫内膜上皮粘附和接受性的关键调节因子。

The human endometrium undergoes dramatic remodeling throughout the menstrual cycle that are essential for successful blastocyst attachment and implantation in the mid-secretory (receptive) phase. microRNA (miR) play a role in the preparation of endometrial receptivity. miR-23b-3p expression is increased in fertile endometrium during receptivity. Here we aimed to investigate miR-23b-3p function during receptivity. qPCR and in situ hybridization were used to investigate the expression and localization of miR-23b-3p in human endometrium, respectively. Ishikawa cells (endometrial epithelial cell line) and endometrial organoid-derived epithelial cells were transfected with miR-23b-3p mimic and trophoblast progenitor spheroid (blastocyst surrogate) adhesion assay was used to determine effects on blastocyst adhesion to endometrial cells. We demonstrated that miR-23b-3p was significantly upregulated in fertile endometrium of the receptive phase compared to the non-receptive, proliferative phase. No difference was identified for the expression of miR-23b-3p between fertile and infertile mid-secretory phase endometrium. miR-23b-3p localized to the epithelium and stroma in the mid-secretory phase but was undetectable in the proliferative phase of fertile endometrium. Functionally, miR-23-3p overexpression in Ishikawa cells and fertile endometrial organoid-derived epithelial cells significantly improved their adhesive capacity to trophoblast progenitor spheroids. miR-23b-3p overexpression in infertile endometrial organoid-derived epithelial cells did not improve adhesion. Among 10 miR predicted gene targets examined, miR-23b-3p overexpression in Ishikawa cells significantly reduced the expression of MET, SFRP4 and ACADSB, compared to control. The reduction of SFRP4 after miR23b-3p overexpression was confirmed by immunoblotting in fertile organoid-derived epithelial cells. SFRP4 expression in fertile endometrium exhibited an inverse expression pattern compared to miR-23b-3p and was higher in the proliferative phase compared to mid-secretory phase. Overall, miR-23b-3p is likely a critical regulator of endometrial epithelial adhesion and receptivity.