MiR-613 suppresses retinoblastoma cell proliferation, invasion, and tumor formation by targeting E2F5

被引:16
|
作者
Zhang, Yiting [1 ]
Zhu, Xinyue [1 ]
Zhu, Xiaomin [2 ]
Wu, Yan [2 ]
Liu, Yajun [1 ]
Yao, Borui [1 ]
Huang, Zhenping [1 ]
机构
[1] Nanjing Univ, Jinling Hosp, Med Sch, Dept Ophthalmol, Nanjing 210002, Jiangsu, Peoples R China
[2] Jinling Hosp, Dept Ophthalmol, Nanjing, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
Retinoblastoma; miR-613; E2F5; HEPATOCELLULAR-CARCINOMA; PATHWAY; CANCER; MICRORNAS; OVEREXPRESSION; CHEMOREDUCTION; EXPRESSION; FAMILY; GROWTH;
D O I
10.1177/1010428317691674
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Retinoblastoma is a common intraocular malignancy that occurs during childhood. MicroRNAs play critical roles in the regulation of retinoblastoma initiation and progression, and aberrant expression of miR-613 had been reported in various types of cancer. However, the role and mechanism of its function in retinoblastoma are still unclear. In this study, we found that miR-613 was downregulated in retinoblastoma tissues and cell lines. Overexpression of miR-613 suppressed retinoblastoma cell proliferation, migration, and invasion and induced cell cycle arrest in vitro. Additionally, overexpressed miR-613 also inhibited tumor formation of retinoblastoma cells in vivo. We further identified E2F5 as a direct target of miR-613. Reintroduction of E2F5 without 3'-untranslated region reversed the inhibitory effects of miR-613 on cell proliferation and invasion. Our data collectively indicate that miR-613 functions as a tumor suppressor in retinoblastoma through downregulating E2F5, supporting the targeting of the novel miR-613/E2F5 axis as a potentially effective therapeutic approach for retinoblastoma.
引用
收藏
页码:1 / 12
页数:12
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