MicroRNA-1/206 Targets c-Met and Inhibits Rhabdomyosarcoma Development

doi:10.1074/jbc.M109.020511

科研成果详情

题名	MicroRNA-1/206 Targets c-Met and Inhibits Rhabdomyosarcoma Development
作者	Yan, Dongsheng 1,2; Dong, Xiang Da 3; Chen, Xiaoyan 1,2; Wang, Lihua 1,2; Lu, Chunjing 1,2; Wang, Jiao1,2; Qu, Jia 1,2; Tu, Lili 1,2
发表日期	2009-10-23
发表期刊	JOURNAL OF BIOLOGICAL CHEMISTRY 影响因子和分区
语种	英语
原始文献类型	Article
关键词	Binding sites Cell culture Cell proliferation Cells Electrophoresis Molecular biology Muscle Tumors Negative control Rhabdomyosarcoma Skeletal muscle Tissue specifics Transient transfection Tumor suppressors Untranslated regions Western-blot analysis
其他关键词	ALVEOLAR RHABDOMYOSARCOMA ; BREAST-CANCER ; EXPRESSION ; CELL ; METASTASIS ; RECEPTOR ; DIFFERENTIATION ; DYSREGULATION ; PAX3 ; MICE
摘要	MicroRNAs (miRNAs) are endogenous short (similar to 22) nucleotide RNAs that regulate gene function by modification of target mRNAs. miRNA-1 (miR-1) and miRNA-206 (miR-206) are highly expressed in skeletal muscle. Due to the tissue-specific nature of miR-1/206 for skeletal muscles, we investigated the role of miR-1/206 in the development of rhabdomyosarcoma. Initially, we demonstrated that miR-1/206 expression was suppressed in rhabdomyosarcomas and found at very low levels in a rhabdomyosarcoma RD cell line. Transient transfection of miR-1/206 into cultured RD cells led to a significant decrease in cell growth and migration. Using bioinformatics, we identified two putative miR-1/206 binding sites within the 3'-untranslated region of the human c-Met mRNA. miR-1/206 was then shown to have activity on mRNA expression by targeting the c-Met 3'-untranslated region. The expression of c-Met protein was shown to be down-regulated by subsequent Western blot analysis. Conversely, up-regulation of c-Met was confirmed in tissue samples of human rhabdomyosarcoma, with its level inversely correlated with miR-1/206 expression. In vivo, miR-1/206-expressing tumor cells showed growth delay in comparison with negative control. Our results demonstrated that miR-1/206 suppressed c-Met expression in rhabdomyosarcoma and could function as a potent tumor suppressor in c-Met-overexpressing tumors. Inhibition of miR-1/206 function could contribute to aberrant cell proliferation and migration, leading to rhabdomyosarcoma development.
资助项目	National Natural Science Foundation of ChinaNational Natural Science Foundation of China (NSFC) [30772385]
出版者	AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
出版地	BETHESDA
ISSN	0021-9258
EISSN	1083-351X
卷号	284 期号:43 页码:29596-29604
DOI	10.1074/jbc.M109.020511
页数	26
WOS类目	Biochemistry & Molecular Biology
WOS研究方向	Biochemistry & Molecular Biology
WOS记录号	WOS:000270896800041
收录类别	SCIE ; EI ; PUBMED ; SCOPUS
EI入藏号	20094512417413
EI主题词	RNA
URL	查看原文
PubMed ID	19710019
PMC记录号	PMC2785592
SCOPUSEID	2-s2.0-70350383632
通讯作者地址	[Qu, Jia]School of Opthalmology and Optometry,Eye Hospital,Wenzhou Medical College,270 Xueyuan Rd.,China
Scopus学科分类	Biochemistry;Molecular Biology;Cell Biology
TOP期刊	TOP期刊
引用统计	被引频次：232[WOS] [WOS记录] [WOS相关记录]
文献类型	期刊论文
条目标识符	https://kms.wmu.edu.cn/handle/3ETUA0LF/8194
专题	温州医科大学
通讯作者	Qu, Jia
作者单位	1.School of Ophthalmology and Optometry,Eye Hospital,Wenzhou Medical College,270 Xueyuan Rd.,China; 2.Key Laboratory of Vision Science,Ministry of Health of the People's Republic of China,Zhejiang Provincial Key Laboratory of Opthalmology and Optometry,China; 3.Department of Surgery,Stamford Hospital,Columbia University,United States
通讯作者单位	眼视光学院（生物医学工程学院）、附属眼视光医院
推荐引用方式 GB/T 7714	Yan, Dongsheng,Dong, Xiang Da,Chen, Xiaoyan,et al. MicroRNA-1/206 Targets c-Met and Inhibits Rhabdomyosarcoma Development[J]. JOURNAL OF BIOLOGICAL CHEMISTRY,2009,284(43):29596-29604.
APA	Yan, Dongsheng., Dong, Xiang Da., Chen, Xiaoyan., Wang, Lihua., Lu, Chunjing., ... & Tu, Lili. (2009). MicroRNA-1/206 Targets c-Met and Inhibits Rhabdomyosarcoma Development. JOURNAL OF BIOLOGICAL CHEMISTRY, 284(43), 29596-29604.
MLA	Yan, Dongsheng,et al."MicroRNA-1/206 Targets c-Met and Inhibits Rhabdomyosarcoma Development".JOURNAL OF BIOLOGICAL CHEMISTRY 284.43(2009):29596-29604.