卵巢癌（OC）是女性最常见的恶性肿瘤之一。环状RNA（circRNAs）有潜力调控OC的发展。因此，本研究调查了circASXL1在OC进展中的作用。通过MTT、克隆形成、划痕愈合和Transwell实验评估了细胞功能。RIP和双荧光酶报告实验确认了miR-320d与circASXL1或RACGAP1之间的关系。MeRIP被用于检测m6A水平。建立了异种移植瘤进行体内实验。OC组织和细胞中circASXL1和RACGAP1水平上升，而miR-320d表达下降。circASXL1的上调与OC患者的不良预后相关。circASXL1沉默抑制了OC细胞的增殖、迁移和侵袭能力，无论在体外还是在体内。在机制上，METTL3/IGF2BP1介导的m6A修饰维持了circASXL1的稳定性并上调了其表达。circASXL1是一个ceRNA，从RACGAP1中分离了miR-320d，导致RACGAP1表达增加。circASXL1通过miR-320d/RACGAP1轴促进了OC细胞的增殖、迁移和侵袭。因此，m6A修饰的circASXL1通过靶向miR-320d并激活RACGAP1/PI3K/Akt途径，在OC中充当了一个致癌基因，为OC诊断提供了新的有前景的生物标记物。© 2023年作者。由牛津大学出版社发表。版权所有。如需权限，请发送电子邮件至：journals.permissions@oup.com。

Ovarian cancer (OC) is one of the most common malignant tumors in women. Circular RNAs (circRNAs) can potentially regulate the development of OC. Therefore, this study investigated the role of circASXL1 in OC progression. Cell functions were assessed by MTT, colony formation, wound healing and transwell assays. RIP and dual luciferase reporter assays confirmed the relationship between miR-320d and circASXL1 or RACGAP1. MeRIP was utilized to detect m6A levels. Xenograft tumor was established for in vivo experiments. CircASXL1 and RACGAP1 levels were increased in OC tissues and cells, whereas miR-320d expression was decreased. Upregulation of circASXL1 was associated with poor prognosis in OC patients. CircASXL1 silencing suppressed OC cell proliferation, migration and invasion in vitro and in vivo. Mechanistically, METTL3/IGF2BP1-mediated m6A modification maintained circASXL1 stability and upregulated its expression. CircASXL1 was a ceRNA that sequestrated miR-320d from RACGAP1, leading to increased RACGAP1 expression. CircASXL1 promoted OC cell proliferation, migration and invasion via the miR-320d/RACGAP1 axis. Therefore, m6A-modified circASXL1 acts as an oncogene in OC by targeting miR-320d and activating RACGAP1/PI3K/Akt pathway, which provides novel promising biomarkers for OC diagnosis.© The Author(s) 2023. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.