Abstract
The long noncoding RNA nuclear-enriched abundant transcript 1 (NEAT1) is reportedly involved in the initiation and progression of cancers of several types. However, the role, expression status, and the detailed mechanism of NEAT1 in retinoblastoma (RB) yet need to be unraveled. We explored the role and the mechanism of NEAT1 activity in RB. Our data show enhanced NEAT1 expression in RB-affected tissues compared with the corresponding control. Functional experiments reveal that a NEAT1 knockdown in RB cells significantly inhibits proliferation, cycle progression, and facilitates apoptosis and caspase-3 and -9 activities. Besides that, miR-124 was predicted to be a target of NEAT1 and its reduced expression, as well as the inverse correlation of NEAT1 with miR-124, was observed in RB-affected tissues. Further, luciferase and RNA immunoprecipitation (RIP) assays confirmed the interaction between NEAT1 and miR-124. Rescue experiments confirmed that the inhibition of miR-124 could reverse the effect of NEAT1 on RB cell proliferation, cycle arrest, apoptosis, and caspase-3 and -9 activities. Thus, NEAT1 promotes RB progression by sponging miR-124, providing a therapeutic target for RB.