Downregulation of MIAT reduces the proliferation and migratory and invasive abilities of retinoblastoma cells by sponging miR-665 and regulating LASP1.

Abstract

Long non-coding RNAs (lncRNAs) can function as onco-lncRNAs in several types of human cancer, including retinoblastoma (Rb). The present study investigated the potential role and regulatory mechanism of the lncRNA myocardial infarction-associated transcript (MIAT) in Rb. To do so, the expression levels of MIAT, microRNA (miR)-665, and LIM and SH3 protein 1 (LASP1) in Rb tissues from patients or Rb cells were analysed using reverse transcription quantitative PCR. The interactions between miR-665 and MIAT/LASP1 were confirmed by the dual-luciferase reporter assay. MTT, Transwell (to assess migration and invasion) and western blotting assays were used to explore the functions of the MIAT/miR-665/LASP1 axis on Rb progression in vitro. The results of the present study indicated that MIAT targeted miR-665. In Rb tissues and cell lines, high expression of MIAT was observed, whereas miR-665 was downregulated in Rb tissues. Furthermore, the proliferation and migratory and invasive abilities of Rb Y79 and HXO-RB44 cells were decreased following MIAT downregulation or miR-665 overexpression. In addition, LASP1 was identified as a target gene of miR-665. Both the decreased expression of miR-665 and the elevated expression of LASP1 reversed the suppressive effects of MIAT knockdown on the proliferation and migratory and invasive abilities of Y79 cells. Furthermore, MIAT silencing attenuated the development of Rb by regulating the miR-665/LASP1 axis. Taken together, these findings suggested that MIAT may be considered as a possible therapeutic target for Rb.