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Retinoblastoma (RB) is the most common intraocular tumor in childhood. Long non-coding RNA (lncRNA) nuclear paraspeckle assembly transcript 1  (NTAT1)  has been reported to be related to RB progression. This study aims to study the molecular mechanism of  NEAT1  in regulating cell cycle, proliferation, apoptosis, migration, and invasion in RB. The expression levels of  NEAT1  and miR-3619-5p were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The protein expression of LIM and SH3 domain protein 1 (LASP1) was measured by western blot. The proliferation of RB cells was analyzed by cell counting kit-8 (CCK-8) and cell colony formation assays. Cell migration and invasion were evaluated by transwell assay. Cell cycle and apoptosis were assessed by flow cytometry analysis. The association between miR-3619-5p and  NEAT1  or LASP1 was predicted by starBase 3.0 database and identified by dual-luciferase reporter assay. The effects of  NEAT1  knockdown on the tumor growth  in vivo  were detected by  in vivo  tumor formation assay.  NEAT1  expression was dramatically up-regulated, and miR-3619-5p expression was obviously downregulated in RB tissues and cells compared with control groups. The protein level of LASP1 was obviously increased in RB tissues or cells relative to paracancerous normal tissues or cells, respectively. Functionally,  NEAT1  silencing inhibited RB cell migration, invasion, and proliferation, whereas induced cell apoptosis and cell cycle arrest in RB; this phenomenon was partially abolished by miR-3619-5p inhibitor. Mechanistically,  NEAT1  acted as a sponge of miR-3619-5p, and miR-3619-5p was associated with LASP1. In addition,  NEAT1  knockdown decreased the volume and weight of RB tumor  in vivo . Together,  NEAT1  silencing repressed cell migration, invasion, and proliferation, whereas induced cell apoptosis and cycle arrest by sponging miR-3619-5p to inhibit LASP1 expression in RB cells. This study may provide a theoretical basis for RB therapy.

LncRNA NEAT1 Knockdown Inhibits Retinoblastoma Progression by miR-3619-5p/LASP1 Axis