shRNA-mediated RPS15A silencing inhibits U937 acute myeloid leukemia cell proliferation and enhances apoptosis

被引:12
|
作者
Li, Guangyao [1 ,2 ]
Zhang, Li [2 ]
Liu, Jizhu [2 ]
Xiao, Taiwu [2 ]
Liu, Guozhen [2 ]
Wang, Jingxia [2 ]
Hou, Ming [1 ]
机构
[1] Shandong Univ, Qilu Hosp, Dept Hematol, 107 Wenhua Xi Rd, Jinan 250012, Shandong, Peoples R China
[2] Liaocheng Peoples Hosp, Dept Hematol, Liaocheng 252000, Shandong, Peoples R China
基金
中国国家自然科学基金;
关键词
acute myeloid leukemia; shRNA; ribosomal protein S15a; proliferation; apoptosis; INCREASES CHEMOSENSITIVITY; DOWN-REGULATION; UP-REGULATION; GENE; EXPRESSION; GROWTH; REVEALS; OVEREXPRESSION; IDENTIFICATION; SUPPRESSION;
D O I
10.3892/mmr.2016.5064
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Ribosomal protein S15a (RPS15A), which is a component of the 40S ribosomal subunit, is able to promote mRNA/ribosome interaction during the early stage of translation. Previous studies have demonstrated that RPS15A regulates cell growth and is involved in several types of human cancer. The aim of the present study was to investigate the role of RPS15A in acute myeloid leukemia (AML). Lentivirus-delivered short hairpin RNA (shRNA) was used to silence RPS15A expression in the U937 AML cell line. Subsequently, the effects of RPS15A silencing on cell viability, cell cycle progression and apoptosis were investigated. The results indicated that RPS15A knockdown significantly inhibited cell growth. Furthermore, flow cytometric analysis demonstrated that the majority of U937 cells were arrested in G(0)/G(1) phase and sub-G(1) phase after RPS15A knockdown, as determined using propidium iodide staining. In addition, U937 cells underwent apoptosis in response to RPS15A silencing, as determined using Annexin V/7-aminoactinomycin D staining. In conclusion, the present study provides novel evidence indicating that RPS15A modulates AML cell growth in vitro, and may be considered a novel therapeutic target for the treatment of AML.
引用
收藏
页码:4400 / 4406
页数:7
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