Long noncoding RNA UCA1 facilitates cell proliferation and inhibits apoptosis in retinoblastoma by activating the PI3K/Akt pathway.

Abstract

BackgroundThis study aimed to explore the effects of the long noncoding RNA (lncRNA)-UCA1 on retinoblastoma (RB) and the potential underlying molecular mechanisms.MethodsThe expression of lncRNA-UCA1 was measured by qRT-RCR in both RB tissues and the RB cell lines HXO-RB44 and Y79. The relationship between lncRNA-UCA1 expression and the clinical characteristics of RB patients was evaluated. Cell proliferation, colony formation, and apoptosis and the cell cycle of HXO-RB44 and Y79 cells were evaluated by the cell counting kit-8 (CCK-8) assay, colony formation assay, and flow cytometry, respectively. In addition, the expression levels of PCNA, caspase-3, survivin, p16, p21, CDK2, PI3K, p-PI3K, Akt, p-Akt, and S6k in HXO-RB44 and Y79 cells were measured by Western blotting.ResultsLncRNA-UCA1 was highly expressed in both RB tissues and the RB cell lines HXO-RB44 and Y79. Moreover, lncRNA-UCA1 expression levels in RB patients were correlated with tumour size, optic nerve invasion, and pathologic grade. LncRNA-UCA1 promoted cell proliferation and cell cycle progression and inhibited apoptosis in HXO-RB44 and Y79 cells. LncRNA-UCA1 overexpression dramatically increased the expression of S6k and the phosphorylation of PI3K and Akt in RB cells. Treatment with the PI3K inhibitor LY294002 reversed the effects of lncRNA-UCA1 on RB cell proliferation, apoptosis, and cell cycle progression.ConclusionsOur study showed that lncRNA-UCA1 could promote cell proliferation and cell cycle progression and inhibit cell apoptosis in RB by activating the PI3K/Akt pathway.