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The aim of the present study was to determine the role of long intergenic non-protein coding RNA 858 (LINC00858) in retinoblastoma (RB) and investigate the underlying molecular mechanisms. RB tissues and paracancerous tissues of 27 RB cases were obtained. RB cell lines (SO-RB50, Y79, HXO-RB44 and WERI-Rb1) and a normal retinal epithelial cell line (ARPE-19) were cultured for in vitro experiments. Batches of SO-RB50 and Y79 cells were assigned to groups transfected with small interfering RNA targeting LINC00858 (si-LINC00858 group), microRNA (miR)-3182 mimics or inhibitor, or the respective controls. A Cell Counting Kit-8 and Transwell assays were performed to assess the effect of the transfections on the proliferation, migration and invasion of SO-RB50 and Y79 cells. A luciferase reporter assay was performed using SO-RB50 cells to demonstrate the direct binding of LINC00858 and miR-3182. Reverse transcription-quantitative PCR was employed to detect LINC00858 and miR-3182 expression. Pearson correlation analysis was used to assess the correlation between the expression of LINC00858 and miR-3182. The results indicated that RB tissues and cells exhibited aberrantly elevated LINC00858 expression (P&lt;0.05). Compared with those in the control-transfected group, SO-RB50 and Y79 cells of the si-LINC00858 group had a lower cell proliferation, as well as a lower number of migrated and invaded cells (all P&lt;0.05). miR-3182 was proven to be a target gene of LINC00858, to be abnormally downregulated in RB tissues and cells (P&lt;0.05) and to be negatively correlated with LINC00858 expression. Compared with those in the si-LINC00858 + inhibitor-negative control group, SO-RB50 and Y79 cells of the si-LINC00858 + miR-3182 inhibitor group exhibited a significantly higher relative proliferation, migration and invasion (all P&lt;0.05). In conclusion, LINC00858 promoted RB cell proliferation, migration and invasion, at least partially by inhibiting miR-3182.

LINC00858 promotes retinoblastoma cell proliferation, migration and invasion by inhibiting miR‑3182