• Jianchang Li, Xiuming Liu, Wenqi Wang, and Chaopeng Li.
• Department of Ophthalmology, The Affiliated Huaian No. 1 People's Hospital of Nanjing Medical University, Huai' an, Jiangsu, China.
• Arch Med Sci. 2020 Jan 1; 16 (4): 941-956.

IntroductionRetinoblastoma (RB) is a malignant tumor that is derived from photoreceptors. It is common in children under 3 years old with a family genetic predisposition. MicroRNA-133a-3p (miR-133a-3p) is one of the tumor-related miRNAs that interprets a critical function in the genesis and development of various tumors. This study investigated the effects and underlying mechanisms of miR-133a-3p in RB.Material And MethodsQuantitative reverse-transcription polymerase chain reaction (qRT-PCR) analysis was used to assess the miR-133a-3p expression in RB tissues and a cell model. MTT assay, western blot, flow cytometry and luciferase reporter assay were performed to evaluate the effect of miR-133a-3p on cell viability, apoptosis and the cell cycle. An RB xenograft model was established to assess the in vivo influence of miR-133a-3p on RB growth.ResultsMiR-133a-3p level was reduced in RB tissues and the cell model (p < 0.01 or p < 0.001). Addition of miR-133a-3p reduced cell viability, and increased apoptosis and cell cycle arrest (p < 0.001). Additionally, CREB1 was identified to be the target of miR-133a-3p in RB cell lines (p < 0.001). Cell viability reduction, apoptosis and cell cycle arrest increases mediated by miR-133a-3p were attenuated by CREB1 overexpression (p < 0.001). MiR-133a-3p inhibited tumor growth of RB in vivo (p < 0.001).ConclusionsOur results reveal that miR-133a-3p exhibits anti-cancer effects by targeting CREB1 in RB. This study provides a new direction for effective targeted treatment of this disease.Copyright © 2019 Termedia & Banach.

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