IR@PKUHSC  > 北京大学第二临床医学院
学科主题临床医学
Ectopic expression of miR-494 inhibited the proliferation, invasion and chemoresistance of pancreatic cancer by regulating SIRT1 and c-Myc
Liu, Y.1; Li, X.1; Zhu, S.1; Zhang, J-G2; Yang, M.1; Qin, Q.1; Deng, S-C1; Wang, B.3; Tian, K.1; Liu, L.1; Niu, Y.1; Wang, C-Y1; Zhao, G.1
刊名GENE THERAPY
2015-09-01
DOI10.1038/gt.2015.39
22期:9页:729-738
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Biochemistry & Molecular Biology ; Biotechnology & Applied Microbiology ; Genetics & Heredity ; Medicine, Research & Experimental
研究领域[WOS]Biochemistry & Molecular Biology ; Biotechnology & Applied Microbiology ; Genetics & Heredity ; Research & Experimental Medicine
关键词[WOS]MICRORNA EXPRESSION ; MICROARRAY ANALYSIS ; FEEDBACK LOOP ; CELLS ; ADENOCARCINOMA ; TUMORIGENESIS ; INACTIVATION ; SENESCENCE ; THERAPY ; TARGET
英文摘要

Recent researches demonstrate that microRNAs (miRNAs) are deregulated in numerous cancers and involved in tumorigenesis, whereas their influences on pancreatic cancer (PC) still need further elucidation. The present research revealed that miR-494 was significantly decreased in PC cell lines and tissues. Functional study showed that overexpressed miR-494 could remarkably inhibit proliferation of PC cells both in vitro and in vivo, which was due to induction of apoptosis, G1-phase arrest and senescence. Moreover, upregulated miR-494 significantly prohibited invasion of PC cells. Meanwhile, both c-Myc and SIRT1 was identified as targets of miR-494 through dual luciferase assay and further confirmed by the reverse correlation between miR-494 and c-Myc/SIRT1 in PC samples. Furthermore, co-transfection with c-Myc-RNAi and SIRT1-RNAi synergistically reduced c-Myc and SIRT1 expression, and inhibited proliferation of PC, which simulated the effects of miR-494 overexpression. On the contrary, co-overexpression of c-Myc and SIRT1 effectively rescued inhibition of overexpressed miR-494 on PC cells. The clinical characteristics further revealed that low miR-494 correlated with larger tumor size, late tumor node metastasis stage, lymphatic invasion, distant metastasis and poor prognosis. In conclusion, the present study indicated that miR-494 might serve as predictor and inhibitor in PC by directy downregulating the loop of c-Myc and SIRT1.

语种英语
WOS记录号WOS:000360895200005
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被引频次:25[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/400002259/59440
专题北京大学第二临床医学院
作者单位1.Huazhong Univ Sci & Technol, Tongji Med Coll, Union Hosp, Pancreat Dis Inst, Wuhan 430022, Hubei Province, Peoples R China
2.Zhejiang Prov Peoples Hosp, Hepatobiliary & Pancreat Surg, Hangzhou, Zhejiang, Peoples R China
3.Peking Univ, Peoples Hosp, Dept Gastroenterol Surg, Beijing 100871, Peoples R China
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Liu, Y.,Li, X.,Zhu, S.,et al. Ectopic expression of miR-494 inhibited the proliferation, invasion and chemoresistance of pancreatic cancer by regulating SIRT1 and c-Myc[J]. GENE THERAPY,2015,22(9):729-738.
APA Liu, Y..,Li, X..,Zhu, S..,Zhang, J-G.,Yang, M..,...&Zhao, G..(2015).Ectopic expression of miR-494 inhibited the proliferation, invasion and chemoresistance of pancreatic cancer by regulating SIRT1 and c-Myc.GENE THERAPY,22(9),729-738.
MLA Liu, Y.,et al."Ectopic expression of miR-494 inhibited the proliferation, invasion and chemoresistance of pancreatic cancer by regulating SIRT1 and c-Myc".GENE THERAPY 22.9(2015):729-738.
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