Background
Long non-coding RNAs (lncRNAs) play critical roles in the occurrence and progression of various tumors, including ovarian cancer (OC). The lncRNA growth arrest-specific transcript 5 (GAS5) has been shown to be an important modulator in the growth and metastasis of OC cells. Our previous studies confirmed that GAS5 was down-regulated in OC; however, the potential underlying molecular mechanism underlying has not yet been elucidated.
Conclusions
Our study identified GAS5 as a ceRNA that can regulate the PTEN/AKT/mTOR axis by sponging miR-96-5p in OC.
Methods
We screened the Gene Expression Profiling Interactive Analysis (GEPIA) database for the expression of the lncRNA GAS5 in OC. Cell Counting Kit-8 (CCK-8), transwell assay, colony formation assay, flow cytometry analysis, and western blotting were applied to determine the various functions of GAS5 in OC progression. The competing endogenous RNA (ceRNA) mechanism was verified through bioinformatics analysis, dual-spectral luciferase reporter gene assay, and RNA immunoprecipitation assay (RIPA). Finally, the expression interactions between microRNA-96-5p, phosphatase and tensin homolog deleted on chromosome ten (PTEN), and GAS5 were measured.
Results
Our results demonstrated decreased expression levels of GAS5 and PTEN in OC samples and cell lines, while miR-96-5p was up-regulated when compared with the controls. GAS5 overexpression could significantly reduce OC cell proliferation and invasion ability via suppression of miR-96-5p expression. Moreover, GAS5 could influence the PTEN/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway. Conclusions: Our study identified GAS5 as a ceRNA that can regulate the PTEN/AKT/mTOR axis by sponging miR-96-5p in OC.