Epithelial ovarian cancer (EOC) accounts for approximately 90% of all ovarian cancer cases and is the most common cause of gynecological cancer death. Understanding the molecular mechanisms of EOC will help develop better diagnostics and more effective treatments. This study aimed to investigate whether long non-coding RNA ADAMTS9-AS1 (ADAMTS9-AS1) could regulate solute carrier family 7 member 11 (SLC7A11) expression and inhibit ferroptosis by sponging micoRNA-587 in EOC progression. Quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting results showed that ADAMTS9-AS1 expression was elevated in EOC cells; microRNA-587 expression was up-regulated and SLC7A11 expression was down-regulated after knocking down ADAMTS9-AS1 by transfection with siRNAs; however, microRNA-587 inhibitor reversed SLC7A11 expression in ADAMTS9-AS1 knocking down cells. Ferroptosis related marker detection and cell function assay confirmed that knocking down ADAMTS9-AS1 inhibited EOC cells proliferation and migration by promoting ferroptosis. Overexpression of micoRNA-587 also promoted ferroptosis while inhibited cells proliferation and migration in EOC cells. Additionally, micoRNA-587 inhibitor reversed the effect of ADAMTS9-AS1 silence on the ferroptosis and cell function. Moreover, dual-luciferase reporter gene assay and RNA immunoprecipitation assay confirmed that miR-587 was as a sponge for ADAMTS9-AS1 and SLC7A11. In conclusion, our study found that ADAMTS9-AS1 attenuated ferroptosis by targeting miR-587/SLC7A11 axis in EOC. Our study provides a new therapeutic target for EOC.
Keywords: Long non-coding RNA ADAMTS9-AS1; epithelial ovarian cancer; ferroptosis; micoRNA-587; solute carrier family 7 member 11.