期刊论文详细信息
Cancer Cell International
MiR-99a may serve as a potential oncogene in pediatric myeloid leukemia
Xuequn Luo1  Hua Zhang3  Yueqin Chen2  Xiaoli Zhang1  Jun Wu2  Yanni Liang1  Libin Huang1  Zhiyong Ke1  Xiaojuan Li2  Lidan Zhang1 
[1] Department of Pediatric, The First Affiliated Hospital of Sun Yat-Sen University, Zhongshan Er Lu, Guangzhou 510080, China;Key Laboratory of Gene Engineering of the Ministry of Education, State Key Laboratory for Biocontrol, Sun Yat-Sen University, Guangzhou 510275, China;China-America Cancer Research Institute, Key Laboratory for Medical Molecular Diagnostics of Guangdong Province, Guangdong Medical College, 1 Xincheng Road, Song-Shan Lake (SSL) Science, Technology and Industrial Park, Dongguan, Guangdong 523808, China
关键词: Childhood;    Myeloid leukemia;    TRIB2;    CTDSPL;    miR-99a;   
Others  :  792667
DOI  :  10.1186/1475-2867-13-110
 received in 2013-07-04, accepted in 2013-11-01,  发布年份 2013
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【 摘 要 】

Background

Leukemia is the most common malignant proliferative disease in children. Our previous study found that miR-99a was up-regulated in pediatric primary AML using microRNA expression profiles. Up to date, although there is a certain number of reports on microRNA expression features and functions in pediatric acute myeloid leukemia (AML) and chronic myeloid leukemia (CML), the expression and function of miR-99a in these diseases remain to be investigated.

Methods

qRT-PCR was performed to measure the expression level of miR-99a in 88 samples including 68 pediatric acute myeloid leukemia patients, 8 chronic myeloid leukemia patients and 12 pediatric controls. MTT assay, apoptosis assay, dual-luciferase reporter transfection assay and western blot analysis were used to investigate the function of miR-99a.

Results

MiR-99a was highly expressed in pediatric-onset AML (M1-M5) and CML, while significantly lowly expressed during complete remission of these diseases. MTT assay indicated that the proliferations of K562 and HL60 cells were significantly promoted by miR-99a, and apoptosis assessment by Annexin V/propidium iodide staining demonstrated that the apoptosis of these cells was inhibited by miR-99a. Additionally, dual-luciferase reporter transfection assay and western blot analysis indicated that miR-99a may target CTDSPL and TRIB2, which are two tumor suppressor genes.

Conclusions

This study revealed that miR-99a may play a potential oncogenic role in pediatric myeloid leukemia including AML and CML via regulating tumor suppressors CTDSPL and TRIB2, suggesting that these two leukemias might share some common biological pathways involved in the generation and development of disease and miR-99a could be a common therapeutic target for myeloid leukemias treatment.

【 授权许可】

   
2013 Zhang et al.; licensee BioMed Central Ltd.

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