Background: Long noncoding RNAs (lncRNAs) are dysregulated and play an important role in the tumorigenesis and progression of cancers. However, the potential roles of SNHG16 in retinoblastoma progression still remain largely unclear.
Materials and methods: The expression levels of SNHG16, miR-182-5p, miR-128-3p and LASP1 in retinoblastoma tissues and cell lines were detected using qRT-PCR. The migratory and invasive abilities of retinoblastoma cells were assessed using Transwell assay. The regulatory relationships among SNHG16, miR-182-5p, miR-128-3p and LASP1 were analyzed through bioinformatics prediction and validated by luciferase reporter assay and Western blot.
Results: Here, we demonstrated that SNHG16 was frequently up-regulated in retinoblastoma tissue samples and cell lines. Clinicopathological features showed that high levels of SNHG16 were significantly associated with retinoblastoma metastasis and predicted poor overall survival. Functional studies demonstrated that knockdown of SNHG16 suppressed retinoblastoma cell migration and invasion. Mechanistic investigation revealed that SNHG16 exerted its oncogenic activity through increasing LASP1 expression and sponging miR-182-5p and miR-128-3p.
Conclusion: Taken together, our findings suggest SNHG16 as a novel biomarker and therapeutic target against retinoblastoma.
Keywords: long noncoding RNA, retinoblastoma, SNHG16, metastasis, LASP1