目的 探讨核因子I-C（NFIC）对子宫内膜癌（EC）转移及转移前微环境的影响。方法 将NFIC 小干扰RNA(siRNA)和过表达质粒分别转染入Ishikawa细胞，通过划痕迁移和Transwell侵袭实验观察NFIC对EC迁移和侵袭的影响。进一步提取敲低NFIC来源的外泌体，观察外泌体能否影响Ishikawa细胞的迁移和侵袭，同时在裸鼠体内和EC细胞中观察外泌体是否影响内皮细胞通透性。通过先注射外泌体形成转移前微环境, 然后再注射Ishikawa细胞的方案，观察敲低NFIC来源的外泌体是否影响Ishikawa细胞的转移。最后通过外泌体小RNA测序揭示外泌体影响内皮细胞通透性的机制。结果 敲低NFIC能增强Ishikawa细胞迁移和侵袭能力。敲低NFIC来源的外泌体能促进原始Ishikawa细胞的迁移和侵袭，同时，通过破坏内皮屏障来促进Ishikawa细胞在裸鼠体内的肠转移。敲低NFIC来源的外泌体中微RNA(miR)-4739含量增加明显，miR-4739能下调HUVEC细胞中多配体蛋白聚糖4（SDC4）的表达，从而增加内皮通透性。结论 NFIC缺失能可通过外泌体中的miR-4739下调内皮细胞SDC4的表达，破坏内皮屏障，从而构建转移前微环境，促进EC细胞的肠转移。

Objective To explore the role of nuclear factor I-C (NFIC) in pre-metastatic niche formation and matastasis in endometrial cancer (EC). Methods NFIC small interfering RNA (siRNA) and overexpression plasmid were transfected into Ishikawa cells respectively to investigate the effect of NFIC on cell migration and invasion through wound healing and Transwell invasion assays. Exosomes derived from NFIC knockdown cells were extracted to investigate the effect on the migration and invasion of Ishikawa cells, observe whether these exosomes could increase endothelial cell permeability in vivo and in vitro, address the effect of pre-injection of these exosomes on the metastasis of Ishikawa cells, and explore the underlying mechanism by small RNA sequencing. Results NFIC knockdown increased the migration and invasion of Ishikawa cells. Exosomes from NFIC knockdown cells increased the migration and invasion of Ishikawa cells, and promoted the metastasis of Ishikawa cells in murine models by destroying barrier function of endothelial monolayer. Furthermore, micro RNA(miR)-4739 level elevated significantly in exosomes from NFIC knockdown cells, and the exosome mediated transfer of miR-4739 could downregulate the expression of syndecan-4（SDC4）, then caused the impairment of endothelial barrier. Conclusion NFIC deficiency in EC cells promotes the formation of pre-metastatic niche through exosome mediated transfer of miR-4739, which downregulates the expression of SDC4 to induce vascular endothelial disruption.