LINC00968 accelerates the progression of epithelial ovarian cancer via mediating the cell cycle progression.

OBJECTIVE: The aim of this study was to clarify the potential role of LINC00968 in the progression of epithelial ovarian cancer (EOC) and the underlying mechanism. PATIENTS AND METHODS: The relative expression level of LINC00968 in EOC tissues (n=40) and normal ovarian tissues (n=40) was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). LINC00968 expression in human-derived ovarian cancer cell lines was examined by qRT-PCR as well. After transfection of LINC00968 small-interfering RNA (siRNA) in ovarian cancer cells, cell cycle progression and cell proliferation were evaluated through flow cytometry, Cell Counting Kit-8 (CCK-8) and colony formation assay, respectively. Tumor xenograft was conducted in nude mice to elucidate the function of LINC00968 in EOC tumorigenesis in vivo. Furthermore, the relative expression levels of cell cycle factors and protein kinase B/extracellular-signal-regulated kinase (AKT/ERK) in ovarian cancer cells influenced by LINC00968 were detected by Western blot. RESULTS: LINC00968 was significantly up-regulated in EOC tissues when compared with normal control tissues. Meanwhile, LINC00968 expression was positively correlated with the prognosis of EOC. Transfection of LINC00968 siRNA in HEY and HO8910 cells markedly attenuated proliferative ability and arrested cell cycle in the G1 phase. Knockdown of LINC00968 remarkably suppressed tumor growth of EOC in nude mice. The silence of LINC00968 significantly downregulated Cyclin D, Cyclin E and CDK4, whereas upregulated p16 and p21. In addition, AKT and ERK pathways were inhibited by knockdown of LINC00968 in ovarian cancer cells. CONCLUSIONS: LINC00968 expression is markedly upregulated in EOC. Meanwhile, it arrests the cell cycle in the G1 phase by inhibiting the ERK and AKT pathways, thus accelerating EOC progression. [ABSTRACT FROM AUTHOR]