MicroRNA-598 acts as an inhibitor in retinoblastoma through targeting E2F1 and regulating AKT pathway

被引:14
|
作者
Liu, Fengge [1 ]
Zhang, Qi [2 ]
Liang, Yan [3 ]
机构
[1] Zoucheng Peoples Hosp, Dept Ophthalmol, Zoucheng, Shandong, Peoples R China
[2] LinQing Peoples Hosp, Dept Ophthalmol, Linqing, Shandong, Peoples R China
[3] Qingdao Univ, Dept Ophthalmol, Med Coll, Affiliated Yantai Yuhuangding Hosp, Yantai 264000, Shandong, Peoples R China
关键词
AKT pathway; miR-598; retinoblastoma; TUMOR-SUPPRESSOR; CELL-PROLIFERATION; CANCER; MIR-598; APOPTOSIS; METASTASIS; INVASION;
D O I
10.1002/jcb.29453
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Recently, microRNAs (miRNAs) receive more attention due to their role in the pathogenesis of malignancies. Retinoblastoma (RB) is the most serious and harmful malignant tumor in infants and young children with eye diseases, which often endangers the lives of children. This study was designed to determine how miR-598 is involved in RB progression. In this study, quantitative reverse transcription-polymerase chain reaction, Western blot, dual-luciferase reporter, Cell Counting Kit-8, and Transwell assays were adopted to detect miR-598 expression and function in RB. The decreased expression of miR-598 was identified in RB. Overexpression of miR-598 suppressed the viability and metastasis of RB cells. Further, E2F transcription factor 1 (E2F1) is verified as a direct target of miR-598. Furthermore, E2F1 recovered miR-598-mediated-inhibition of cell viability and metastasis in RB. In addition, miR-598 was found to promote cell apoptosis and inactivate the protein kinase B (AKT) pathway in RB. miR-598 suppressed RB cell viability and metastasis through inhibiting E2F1 and inactivating AKT pathway, which may provide a new perspective for RB treatment.
引用
收藏
页码:2294 / 2302
页数:9
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