中国科学院机构知识库网格
Chinese Academy of Sciences Institutional Repositories Grid
MicroRNA-125a inhibits cell growth by targeting glypican-4

文献类型:期刊论文

作者Feng, Chao1,2; Li, Jie2; Ruan, Jinlan1; Ding, Kan2
刊名GLYCOCONJUGATE JOURNAL
出版日期2012-10
卷号29期号:7页码:503-511
关键词miR-125a glypican-4 ERK1/2 AKT
ISSN号0282-0080
DOI10.1007/s10719-012-9387-0
文献子类Article
英文摘要Heparan sulfate proteoglycan (HSPG), such as glypican, plays a role as a co-receptor for growth factor to influence cells proliferation. However the mechanism is still vague. Micro-RNAs (miRNAs) regulate cell proliferation. Their capacity to direct the translation and stability of targeted transcripts can dramatically influence cellular physiological function. To explore how the function of glypican is regulated involved in cell proliferation, glypican-4 was chosen with a bioinformatics search identifying targeting seed sequences for miR-125a within the 3'-untranslated regions (3'UTR). Indeed, luciferase constructs containing the 3'UTR of glypican-4 demonstrated around 54 % less activity in miR-125a expressing cells relative to the controls. The expression of glypican-4 at both the transcript and protein level was down-regulated by transition trasfection of miR-125a in the human embryonic kidney cell line 293T (HEK293T). Although cell proliferation of HEK293T was not influenced by the silence of glypican-4, DNA synthesis in response to FGF2 in the cells was attenuated by knockdown of glypican-4 using siRNA technique. Further study showed that phosphorylation of ERK1/2 and AKT was suppressed by overexpressing miR-125a, whereas the suppressed MAPK and AKT signaling could be recovered by anti-miR-125a treatment. Both DNA synthesis and cell proliferation were impaired by the inhibitor of ERK1/2 signaling. MTT assay demonstrated that the cell proliferation was impaired by miR-125a overexpression, however, rescued by anti-miR-125a in HEK293T cells. These results disclosed new function of miR-125a by targeting gene glypican-4 in cell growth process and illustrated the feasibility of using miRNAs as a therapeutic strategy to suppress cells proliferation.
WOS关键词HEPARAN-SULFATE PROTEOGLYCANS ; CANCER-CELLS ; PHOSPHORYLATION ; FIBROBLASTS ; SYNDECAN-1 ; GENES
资助项目National Natural Science Foundation of China (NSFC)[81171914] ; National Science Fund for Distinguished Young Scholars in China[81125025]
WOS研究方向Biochemistry & Molecular Biology
语种英语
WOS记录号WOS:000308356000005
出版者SPRINGER
源URL[http://119.78.100.183/handle/2S10ELR8/277930]  
专题药理学第三研究室
通讯作者Ding, Kan
作者单位1.Huazhong Univ Sci & Technol, Tongji Med Ctr, Coll Pharm, Hubei Key Lab Nat Med Chem & Resource Evaluat, Wuhan 430030, Peoples R China
2.Chinese Acad Sci, Shanghai Inst Mat Med, Glycochem & Glycobiol Lab, Shanghai 201203, Peoples R China;
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GB/T 7714
Feng, Chao,Li, Jie,Ruan, Jinlan,et al. MicroRNA-125a inhibits cell growth by targeting glypican-4[J]. GLYCOCONJUGATE JOURNAL,2012,29(7):503-511.
APA Feng, Chao,Li, Jie,Ruan, Jinlan,&Ding, Kan.(2012).MicroRNA-125a inhibits cell growth by targeting glypican-4.GLYCOCONJUGATE JOURNAL,29(7),503-511.
MLA Feng, Chao,et al."MicroRNA-125a inhibits cell growth by targeting glypican-4".GLYCOCONJUGATE JOURNAL 29.7(2012):503-511.

入库方式: OAI收割

来源:上海药物研究所

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