学科主题临床医学
MicroRNAs-372/373 Promote the Expression of Hepatitis B Virus Through the Targeting of Nuclear Factor I/B
Guo, Hongyan1,2; Liu, Haiying1,2; Mitchelson, Keith1,2,3; Rao, Huiying4; Luo, Mingyong2; Xie, Lan1,2; Sun, Yimin2,3; Zhang, Liang2; Lu, Ying1,2; Liu, Ruyu4; Ren, Aihui2,3; Liu, Shuai2,3; Mou, Shaozhen2,3; Zhu, Jiye5; Zhou, Yuxiang1,2; Huang, Ailong6; Wei, Lai4; Guo, Yong1,2; Cheng, Jing1,2,7
刊名HEPATOLOGY
2011-09-01
DOI10.1002/hep.24441
54期:3页:808-819
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Gastroenterology & Hepatology
资助者National High Technology Program of China ; National Natural Science Foundation of China ; Tsinghua Yu-Yuan Medical Sciences Fund, China ; National High Technology Program of China ; National Natural Science Foundation of China ; Tsinghua Yu-Yuan Medical Sciences Fund, China
研究领域[WOS]Gastroenterology & Hepatology
关键词[WOS]HEPATOCELLULAR-CARCINOMA ; FACTOR-I ; MICRORNA EXPRESSION ; PATIENT SURVIVAL ; GENE-EXPRESSION ; SUPPRESSOR GENE ; CELLULAR FACTOR ; ENHANCER ; TRANSCRIPTION ; REPLICATION
英文摘要

MicroRNAs (miRNAs) play important roles in the posttranscriptional regulation of gene expression. Recent evidence has indicated the pathological relevance of miRNA dysregulation in hepatitis virus infection; however, the roles of microRNAs in the regulation of hepatitis B virus (HBV) expression are still largely unknown. In this study we identified that miR-373 was up-regulated in HBV-infected liver tissues and that the members of the miRs-371-372-373 (miRs-371-3) gene cluster were also significantly co-up-regulated in HBV-producing HepG2.2.15 cells. A positive in vivo association was identified between hepatic HBV DNA levels and the copy number variation of the miRs-371-3 gene cluster. The enhanced expression of miRs-372/373 stimulated the production of HBV proteins and HBV core-associated DNA in HepG2 cells transfected with 1.3 X HBV. Further, nuclear factor I/B (NFIB) was identified to be a direct functional target of miRs-372/373 by in silico algorithms and this was subsequently confirmed by western blotting and luciferase reporter assays. Knockdown of NFIB by small interfering RNA (siRNA) promoted HBV expression, whereas rescue of NFIB attenuated the stimulation in the 1.3 x HBV-transfected HepG2 cells. Conclusion: Our study revealed that miRNA (miRs-372/373) can promote HBV expression through a pathway involving the transcription factor (NFIB). This novel model provides new insights into the molecular basis in HBV and host interaction. (HEPATOLOGY 2011;54:808-819)

语种英语
所属项目编号2006AA020701 ; 30900061/C010803
资助者National High Technology Program of China ; National Natural Science Foundation of China ; Tsinghua Yu-Yuan Medical Sciences Fund, China ; National High Technology Program of China ; National Natural Science Foundation of China ; Tsinghua Yu-Yuan Medical Sciences Fund, China
WOS记录号WOS:000294738300009
引用统计
被引频次:59[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/400002259/66790
专题北京大学第二临床医学院_北京大学肝病研究所
作者单位1.Natl Engn Res Ctr Beijing Biochip Technol, Beijing, Peoples R China
2.CapitalBio Corp, Beijing, Peoples R China
3.Tsinghua Univ, Sch Med, Med Syst Biol Res, Dept Biomed Engn, Beijing 100084, Peoples R China
4.Peking Univ, Peoples Hosp, Inst Hepatol, Beijing 100871, Peoples R China
5.Peking Univ, Peoples Hosp, Ctr Hepatobiliaty Surg, Beijing 100871, Peoples R China
6.Chongqing Med Univ, Educ Minist Infect Dis, Key Lab, Chongqing, Peoples R China
7.Tsinghua Univ, State Key Lab Biomembrane & Membrane Biotechnol, Beijing 100084, Peoples R China
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Guo, Hongyan,Liu, Haiying,Mitchelson, Keith,et al. MicroRNAs-372/373 Promote the Expression of Hepatitis B Virus Through the Targeting of Nuclear Factor I/B[J]. HEPATOLOGY,2011,54(3):808-819.
APA Guo, Hongyan.,Liu, Haiying.,Mitchelson, Keith.,Rao, Huiying.,Luo, Mingyong.,...&Cheng, Jing.(2011).MicroRNAs-372/373 Promote the Expression of Hepatitis B Virus Through the Targeting of Nuclear Factor I/B.HEPATOLOGY,54(3),808-819.
MLA Guo, Hongyan,et al."MicroRNAs-372/373 Promote the Expression of Hepatitis B Virus Through the Targeting of Nuclear Factor I/B".HEPATOLOGY 54.3(2011):808-819.
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