Department of Ophthalmology, Luoyang Central Hospital Affiliated to Zhengzhou University, Luoyang, 471000, China.
Department of Ophthalmology, Luoyang Central Hospital Affiliated to Zhengzhou University, Luoyang, 471000, China.
Exp Cell Res. 2020 Aug 15;393(2):112087. doi: 10.1016/j.yexcr.2020.112087. Epub 2020 May 11.
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.
大量证据表明，长非编码 RNA（lncRNA）在视网膜母细胞瘤（RB）的发生中起作用。然而，lncRNA ILF3-AS1 在 RB 中的作用仍不清楚。在本研究中，我们的工作表明，lncRNA ILF3-AS1 在 RB 组织和细胞系中均增加。ILF3-AS1 的抑制抑制了 RB 细胞在体外的增殖和侵袭。ILF3-AS1 还促进了体内肿瘤的生长。在探索 RB 中 ILF3-AS1 的机制时，我们发现 ILF3-AS1 与 miR-132-3p 结合，miR-132-3p 在 RB 组织中的表达水平较低，并减弱了 RB 的进展。此外，SMAD2 被确认为 miR-132-3p 的靶标。最后，我们发现 SMAD2 的过表达或 miR-132-3p 抑制剂恢复了 ILF3-AS1 抑制对 RB 进展的抑制作用。总之，这些数据表明，ILF3-AS1 通过 miR-132-3p/SMAD2 轴参与 RB 的进展，为 RB 的治疗提供了一个新的有前途的生物标志物。
