MicroRNA‑330 is downregulated in retinoblastoma and suppresses cell viability and invasion by directly targeting ROCK1.

Abstract

Abnormal expression of microRNAs(miRNAs/miRs) has been previously reported in various types of human cancer, such as retinoblastoma(RB). Dysregulated miRNAs have been demonstrated to be important epigenetic regulators of numerous biological events associated with RB. Therefore, improved understanding of the precise roles of miRNAs in RB is required to develop novel therapeutic strategies for the treatment of patients with this disease. In the present study, reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) was performed to detect miR‑330 expression in RB tissues and cell lines. The effects of miR‑330 overexpression on the viability and invasion of RB cells were determined using MTT and Matrigel®‑based invasion assays, respectively. The mechanisms underlying the activity of miR‑330 in RB cells were investigated via bioinformatics analysis, luciferase reporter assays, and RT‑qPCR and western blot analyses. It was revealed that the levels of miR‑330 expression were significantly downregulated in RB tissues and cell lines compared with in control healthy tissues and cells, respectively. Overexpression of miR‑330 in RB cells significantly reduced the viability and invasion of cells invitro. Additionally, ρ‑associated coiled‑coil containing protein kinase1(ROCK1) was identified as a putative target of miR‑330 using bioinformatics analysis. Subsequent experiments revealed that miR‑330 interacted with the 3'‑untranslated region of ROCK1 and downregulated its expression in RB cells. Furthermore, the expression levels of ROCK1 were increased in RB tissues compared with healthy controls and negatively correlated with miR‑330 expression. Finally, upregulation of ROCK1 expression reversed the miR‑330‑induced inhibition of the viability and invasion of RB cells. Collectively, these results suggested that miR‑330 exhibits tumor‑suppressor activity in the development of RB by directly targeting ROCK1, indicating that restoration of miR‑330 expression may be a promising therapeutic technique in the treatment of patients with RB.