MicroRNA-101-3p inhibits proliferation in retinoblastoma cells by targeting EZH2 and HDAC9

作者：Jin, Qifang^*; He, Wenfeng; Chen, Leifeng; Yang, Yang; Shi, Ke; You, Zhipeng^*

来源：Experimental and Therapeutic Medicine, 2018, 16(3): 1663-1670.

DOI：10.3892/etm.2018.6405

• microRNA-101-3p
• retinoblastoma
• proliferation
• enhancer of zeste homolog 2
• histone deacetylase 9

Retinoblastoma is the most frequent intraocular malignant tumor type to occur in childhood. MicroRNA (miR)-101-3p has been reported to function as a tumor suppressor in various types of cancer. However, the biological function and underlying mechanisms of miR-101-3p in retinoblastoma are largely unknown. In the present study, it was identified that miR-101-3p was downregulated in retinoblastoma. MTT and flow cytometry assays demonstrated that ectopic overexpression of miR-101-3p significantly inhibited cell viability and cell cycle progression in WERI-Rb-1 and Y79 cells. In vivo mouse experiments further confirmed the anti-proliferative role of miR-101-3p in retinoblastoma. Additionally, predictions with TargetScan software indicated that the 3-untranslated regions of enhancer of zeste homolog 2 (EZH2) and histone deacetylase (HDAC9) mRNAs are targeted by miR-101-3p. Accordingly, a dual luciferase reporter gene assay demonstrated that miR-101-3p directly targeted EZH2 and HDAC9 to suppress the proliferation of retinoblastoma cells. Meanwhile, the restoration of EZH2 or HDAC9 expression countered the anti-proliferative effect of miR-101-3p on WERI-Rb-1 and Y79 cells. Collectively, these data highlight the role of miR-101-3p in the tumorigenesis of retinoblastoma, and indicate its suitability as a novel therapeutic target.

• 出版日期2018-9
• 单位南昌大学