Abstract
Ovarian cancer is one of the three major gynecological malignancies. It has been reported that Icariside II was able to block the occurrence and development of ovarian cancer. However, the detailed mechanism by which Icariside II regulates the development of ovarian cancer is widely unknown. EdU staining and transwell assays were applied to detect the proliferation, migration, and invasion of ovarian cancer cells. Next, the relationship between miR-144-3p and IGF2R was verified by the dual-luciferase reporter assay. Moreover, in vivo animal model was constructed to verify the effect of Icariside II on the development of ovarian cancer. Icariside II notably inhibited the proliferation, migration, and invasion and induced the apoptosis of ovarian cancer cells. Additionally, Icariside II markedly increased the level of miR-144-3p in ovarian cancer cells. Moreover, IGF2R was targeted by miR-144-3p directly. Icariside II significantly decreased the expression of IGF2R and the phosphorylation level of AKT and mTOR in ovarian cancer cells, which were partially reversed by miR-144-3p inhibitor. Meanwhile, Icariside II remarkably promoted the autophagy of ovarian cancer cells, as confirmed by the increased expression of Beclin-1 and ATG-5 and decreased expression of p62; however, co-treatment with miR-144-3p inhibitor notably decreased autophagy. Furthermore, the result of animal study suggested Icariside II notably inhibited ovarian tumor growth as well. Collectively, Icariside II could suppress the tumorigenesis and development of ovarian cancer by promoting autophagy via miR-144-3p/IGF2R axis. These results may be beneficial for future studies on the use of Icariside II to treat ovarian cancer.