Background
Long non-coding RNAs (lncRNAs) have been reported to play crucial regulatory roles in cellular activities and are associated with the carcinogenesis of various diseases. OIP5-AS1, as a novel lncRNA, function in epithelial ovarian cancer (EOC) still remains unclear. Material and
Conclusion
OIP5-AS1 regulated ovarian cancer progression via modulating miR-137/ZNF217 signaling, suggesting that targeting OIP5-AS1 could be conducive to EOC clinical treatment.
Material and methods
qRT-PCR and Western blot analyses were performed to measure relevant expression, as needed. A series of functional experiments were performed to determine the role of OIP5-AS1 in EOC cells. Luciferase report, RNA pull down and RIP assays were performed to testify the interaction between relevant RNAs.
Methods
qRT-PCR and Western blot analyses were performed to measure relevant expression, as needed. A series of functional experiments were performed to determine the role of OIP5-AS1 in EOC cells. Luciferase report, RNA pull down and RIP assays were performed to testify the interaction between relevant RNAs.
Results
We found that OIP5-AS1 was significantly overexpressed in EOC. Knockdown of OIP5-AS1 inhibited cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) process, yet facilitated apoptosis in vitro. OIP5-AS1 functioned as a competing endogenous RNA (ceRNA) to elevate ZNF217 expression through sponging miR-137. Furthermore, miR-137 inhibition and ZNF217 upregulation can reverse the effects of silencing OIP5-AS1 on the cellular activities of ovarian cancer cells. Also, depleted OIP5-AS1 hindered tumor growth and metastasis in vivo.