JOURNAL ARTICLE

miR-133a-3p promotes apoptosis and induces cell cycle arrest by targeting CREB1 in retinoblastoma

Jianchang Li, Xiuming Liu, Wenqi Wang, Chaopeng Li
Archives of Medical Science: AMS 2020, 16 (4): 941-956
32542098

Introduction: Retinoblastoma (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 methods: Quantitative 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.

Results: MiR-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).

Conclusions: Our 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.

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