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学科主题临床医学
Loss of Repression of HuR Translation by miR-16 May Be Responsible for the Elevation of HuR in Human Breast Carcinoma
Xu, Fang1; Zhang, Xiaotian1; Lei, Yutao2; Liu, Xinwen1; Liu, Zhenyun1; Tong, Tanjun1; Wang, Wengong1
关键词Mir-16 Hur Translational Regulation Breast Carcinoma
刊名JOURNAL OF CELLULAR BIOCHEMISTRY
2010-10-15
DOI10.1002/jcb.22762
111期:3页:727-734
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Biochemistry & Molecular Biology ; Cell Biology
资助者Major State Basic Research Development Program of China ; National Science Foundation of China ; Ministry of Education of People&prime ; s Republic of China ; Major State Basic Research Development Program of China ; National Science Foundation of China ; Ministry of Education of People&prime ; s Republic of China
研究领域[WOS]Biochemistry & Molecular Biology ; Cell Biology
关键词[WOS]BINDING PROTEIN HUR ; INCREASED CYCLOOXYGENASE-2 EXPRESSION ; ENDOTHELIAL GROWTH-FACTOR ; MESSENGER-RNA ; CANCER CELLS ; REPLICATIVE SENESCENCE ; OVARIAN-CARCINOMA ; DEPENDENT MANNER ; DOWN-REGULATION ; STABILIZATION
英文摘要

Elevated levels of RNA binding protein HuR were found in various human cancers. However, the mechanisms underlying HuR overexpression in cancers have not been fully elucidated. Here, we show that miR-16 acts as a novel post-transcriptional regulator for HuR. Knockdown of miR-16 increased HuR protein levels in MDA-MB-231 cells, while over-expression of pre-miR16 reduced HuR expression. Neither knockdown nor over-expression of miR-16 could alter the mRNA levels of HuR. Instead, knockdown of miR-16 increased the level of de novo synthesized HuR protein. Importantly, mechanistic studies showed that miR-16 associated with the 3`UTR of HuR, and knockdown of miR-16 markedly increased the luciferase activity of a HuR 3`UTR-containing reporter. We further demonstrate that the level of miR-16 was inversely correlated with HuR protein level in human breast carcinoma. Together, our results suggest an important role of miR-16 in regulating HuR translation and link this regulatory pathway to human breast cancer. J. Cell. Biochem. 111: 727-734, 2010. (c) 2010 Wiley-Liss, Inc.

语种英语
所属项目编号2007CB507400 ; 30672202 ; 30621002 ; 30770442 ; 30973147 ; B07001
资助者Major State Basic Research Development Program of China ; National Science Foundation of China ; Ministry of Education of People&prime ; s Republic of China ; Major State Basic Research Development Program of China ; National Science Foundation of China ; Ministry of Education of People&prime ; s Republic of China
WOS记录号WOS:000282559200023
引用统计
被引频次:38[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/49923
专题北京大学第三临床医学院_普通外科
作者单位1.Peking Univ, Hlth Sci Ctr, Dept Biochem & Mol Biol, Beijing 100191, Peoples R China
2.Peking Univ, Hosp 3, Dept Surg, Beijing 100191, Peoples R China
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GB/T 7714
Xu, Fang,Zhang, Xiaotian,Lei, Yutao,et al. Loss of Repression of HuR Translation by miR-16 May Be Responsible for the Elevation of HuR in Human Breast Carcinoma[J]. JOURNAL OF CELLULAR BIOCHEMISTRY,2010,111(3):727-734.
APA Xu, Fang.,Zhang, Xiaotian.,Lei, Yutao.,Liu, Xinwen.,Liu, Zhenyun.,...&Wang, Wengong.(2010).Loss of Repression of HuR Translation by miR-16 May Be Responsible for the Elevation of HuR in Human Breast Carcinoma.JOURNAL OF CELLULAR BIOCHEMISTRY,111(3),727-734.
MLA Xu, Fang,et al."Loss of Repression of HuR Translation by miR-16 May Be Responsible for the Elevation of HuR in Human Breast Carcinoma".JOURNAL OF CELLULAR BIOCHEMISTRY 111.3(2010):727-734.
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