Abstract
A great deal of evidence suggests that long non-coding RNAs (lncRNAs) function in the tumorigenesis of retinoblastoma (RB). However, the roles of lncRNA ILF3-AS1 in RB are still unclear. In the present study, our work revealed that the lncRNA ILF3-AS1 was increased in both RB tissues and cell lines. Repression of ILF3-AS1 suppressed both RB cell proliferation and invasion in vitro. ILF3-AS1 also promoted tumor growth in vivo. While exploring the mechanisms behind ILF3-AS1 in RB, we identified that ILF3-AS1 sponges with miR-132–3p that is expressed at low levels in RB tissues as well as attenuates RB progression. Furthermore, SMAD2 was confirmed to be a miR-132–3p target. Finally, we found that SMAD2 overexpression or miR-132–3p inhibitors recover the inhibitory effects of ILF3-AS1 suppression on RB progression. Collectively, these data indicate that ILF3-AS1 is involved in RB progression through the miR-132–3p/SMAD2 axis, providing a novel and promising biomarker that can be used for the treatment of RB.
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