Background: Ovarian cancer is one of the malignant tumors attacking the female reproductive system. Currently, increasing studies have clearly determined the importance of long non-coding RNAs (lncRNAs) in various human cancers including ovarian cancer. However, the role and in-depth mechanism of ubiquitin specific peptidase 2 antisense RNA 1 (USP2-AS1) in ovarian cancer have been not reported yet.
Purpose: We were absorbed into exploring the character of USP2-AS1 in ovarian cancer.
Methods: RT-qPCR analysis reflected gene expression. The GEPIA database provided further evidences, and bioinformatics tools analyzed the potential molecules downstream USP2-AS1 in ovarian cancer. The changes on ovarian cancer cellular functions were assessed via EdU, TUNEL, JC-1 and transwell assays. RNA pull down, RIP and luciferase reporter assays estimated molecule interactions.
Results: USP2-AS1 was obviously up-regulated in ovarian cancer tissues and cell lines. Inhibiting USP2-AS1 had anti-proliferation, pro-apoptosis, and anti-migration effects on ovarian cancer cells. Furthermore, we confirmed that USP2-AS1 sequestered miR-520d-3p to enhance KIAA1522. In addition, miR-520d-3p silence reversed the effect of depleted USP2-AS1 on ovarian cancer cellular behaviors, while such reversion was then abolished by KIAA1522 knockdown.
Conclusion: USP2-AS1 facilitated ovarian cancer progression via miR-520d-3p/KIAA1522 axis, implying USP2-AS1 as a new perspective for the treatment of ovarian cancer.
Keywords: USP2-AS1, miR-520d-3p, KIAA1522, ovarian cancer