FUT8-AS1 promotes ovarian cancer progression and invasion via regulation of miR-149-5p/Notch1 axis

Ovarian cancer (OV) is one of the commonest gynecological malignancies with high mortality and poor prognosis. Recently, long non-coding RNAs (lncRNAs) have been recognized as important regulators of cancer initiation and progression. The purpose of this research was to reveal the role and mechanism of FUT8-AS1 on the growth and metastasis of OV cells. The effect of FUT8-AS1 on cell viability, proliferation and invasion was determined by cell counting kit-8 (CCK-8), Colony formation, Transwell analysis, respectively. Gene Expression Profiling Interactive Analysis (GEPIA) database indicated that FUT8-AS1 was up-regulated in OV tissue samples, and it was also up-regulated in ovarian cancer tissues(n = 32). Patients with low FUT8-AS1 expression had a longer overall survival. FUT8-AS1 was also higher than normal ovarian IOSE-80 cells. Further studies displayed that the silencing of FUT8-AS1 not only significantly inhibited the proliferation and metastasis of OV cells, but also regulated the expression of epithelial-mesenchymal transition (EMT). Subsequently, StarBase 3 and luciferase reporter verified that miR-149-5p could bind to FUT8-AS1. In addition, miR-149-5p inhibitor can significantly enhance cell viability, proliferation and cell invasion, and promote the occurrence of EMT, but these effects disappeared after transfection of FUT8-AS1 siRNA. Importantly, we identified that miR-149-5p could regulate Notch1 in OV cells. Down-regulation of FUT8-AS1 reverses the regulation of Notch 1 in OV cells. Furthermore, the vivo tumor experiments showed that FUT8-AS1 shRNA could reduce tumor volume compared with control group, it also could reduce cell proliferation and increase cell apoptosis by Ki67 and Tunel. These results suggest that FUT8-AS1 promotes OV cell progression and invasion by regulating miR-149-5p/Notch1 axis.