子宫内膜癌（EC）是常见的妇科恶性肿瘤。CircRNA在癌症进展和转移中发挥着关键作用。然而，在EC中circRNA的生物功能仍然大多未知。通过定量实时聚合酶链反应和Western blot分析了EC组织或细胞系中的CircSMAD2、miR-1277-5p、MFGE8和相关标记蛋白表达。进行了体外和体内功能实验，包括EDU、CCK8、集落形成、转移孔、管形成和肿瘤异种移植实验，以探索circSMAD2对EC的影响。通过机制实验确认miR-1277-5p与circSMAD2或MFGE8表达之间的结合。结果发现，EC组织和细胞系中CircSMAD2的上调。在体外，沉默circSMAD2显著抑制EC细胞系的增殖、迁移、侵袭和血管生成。在机制上，circSMAD2 sponge了miR-1277-5p来上调MFGE8的表达。EC组织和细胞系中都观察到了miR-1277-5p的降低和MFGE8的增加。接着，MFGE8的沉默或miR-1277-5p的上调抑制了EC细胞的致癌生物行为。复苏实验显示miR-1277-5p mimics countervailed circSMAD2沉默对EC的抗癌效果。此外，MFGE8过表达也减弱了EC中miR-1277-5p mimics对抑制作用的影响。此外，circSMAD2的沉默也抑制了EC的生长。因此，CircSMAD2通过miR-1277-5p/MFGE8轴在促进EC进展中起着致癌基因的作用。 © 2023年亚洲妇科肿瘤学会，韩国妇科肿瘤学会和日本妇科肿瘤学会。

Endometrial cancer (EC) is a common gynecological malignant tumor. CircRNAs play crucial roles in cancer progression and metastasis. However, the biological functions of circRNAs in EC remain largely unknown.CircSMAD2, miR-1277-5p, MFGE8 and relative maker protein expression in EC tissues or cell lines were analyzed by quantitative real-time polymerase chain reaction and Western blot. In vitro and in vivo functional assays, including EDU, CCK8, colony formation, transwell, tube formation and tumor xenograft assays, were conduct to explore the effects of circSMAD2 on EC. Mechanism assays were conducted to confirm the binding between miR-1277-5p and circSMAD2 or MFGE8 expression.Upregulation of circSMAD2 was uncovered in both EC tissues and cell lines. Functionally, silencing of circSMAD2 apparently inhibited the proliferation, migration, invasion and angiogenesis of EC cell lines in vitro. Mechanistically, circSMAD2 sponged miR-1277-5p to upregulate MFGE8 expression. The decrease of miR-1277-5p and increase of MFGE8 were observed both in EC tissues and cell lines. Then MFGE8 knockdown or miR-1277-5p upregulation suppressed EC cell oncogenic biological behavior. Rescue experiments showed that miR-1277-5p mimics countervailed the anticancer effects of circSMAD2 silencing on EC. Besides that, MFGE8 overexpression also attenuated the inhibitory action of miR-1277-5p mimic in EC. Moreover, knockdown of circSMAD2 inhibited EC growth in vivo.CircSMAD2 functions as an oncogene in promoting the progression of EC through miR-1277-5p/MFGE8 axis.© 2023. Asian Society of Gynecologic Oncology, Korean Society of Gynecologic Oncology, and Japan Society of Gynecologic Oncology.