Abstract
A long noncoding RNA called small nucleolar RNA host gene 14 (SNHG14) has been validated as a key regulator of cellular processes in multiple types of human cancer. However, to the best of our knowledge, the expression status and specific roles of SNHG14 in retinoblastoma (RB) have not been studied. The aims of the present study were to determine the expression status of SNHG14 in RB, assess the effects of SNHG14 on malignant characteristics of RB cells and investigate the mechanisms of action of SNHG14 in RB. SNHG14 expression levels in RB tissue samples and cell lines were measured by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). Cell proliferation, apoptosis, migration and invasion in vitro, and tumor growth in vivo were quantitated by the Cell Counting Kit‑8 assay, flow cytometry, migration and invasion assays, and mouse tumor xenograft experiments, respectively. The target microRNA (miRNA) of SNHG14 was predicted by bioinformatics analysis and was subsequently validated by a luciferase reporter assay, RNA immunoprecipitation (RIP) assay, RT‑qPCR, and western blot analysis. SNHG14 was identified to be significantly overexpressed in RB tissues and cell lines. SNHG14 overexpression was markedly associated with the intraocular international retinoblastoma classification stage, optic nerve invasion, and differentiation grade among patients with RB. The patients in the SNHG14 high‑expression group exhibited shorter overall survival compared with the SNHG14 low‑expression group. Functional analysis revealed that SNHG14 silencing inhibited cell proliferation, migration and invasion, and increased apoptosis in vitro, and decreased tumor growth in vivo. SNHG14 directly interacted with, and functioned as a competing endogenous RNA (ceRNA) of, miR‑124, consequently upregulating signal transducer and activator of transcription 3 (STAT3). miR‑124 inhibition and STAT3 expression recovery attenuated the effects of the SNHG14 silencing on RB cells. In conclusion, SNHG14 served as a ceRNA to upregulate STAT3 by sponging miR‑124. Therefore, targeting the SNHG14/miR‑124/STAT3 pathway may be an effective therapeutic strategy against RB.