IR@PKUHSC  > 北京大学深圳医院
学科主题临床医学
CFTR suppresses tumor progression through miR-193b targeting urokinase plasminogen activator (uPA) in prostate cancer
Xie, C.1; Jiang, X. H.1,2; Zhang, J. T.1; Sun, T. T.1; Dong, J. D.1; Sanders, A. J.3; Diao, R. Y.1,4; Wang, Y.1; Fok, K. L.1; Tsang, L. L.1; Yu, M. K.1; Zhang, X. H.1; Chung, Y. W.1; Ye, L.3; Zhao, M. Y.1; Guo, J. H.1; Xiao, Z. J.1; Lan, H. Y.5; Ng, C. F.6; Lau, K. M.7; Cai, Z. M.4; Jiang, W. G.3; Chan, H. C.1,2,8
关键词Cftr Mir-193b Upa
刊名ONCOGENE
2013-05-01
DOI10.1038/onc.2012.251
32期:18页:2282-2291
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Biochemistry & Molecular Biology ; Oncology ; Cell Biology ; Genetics & Heredity
资助者Focused Investment Scheme of the Chinese University of Hong Kong and National 973 project ; Fundamental Research Funds for the Central Universities (JiNan University) ; Focused Investment Scheme of the Chinese University of Hong Kong and National 973 project ; Fundamental Research Funds for the Central Universities (JiNan University)
研究领域[WOS]Biochemistry & Molecular Biology ; Oncology ; Cell Biology ; Genetics & Heredity
关键词[WOS]TRANSMEMBRANE CONDUCTANCE REGULATOR ; CYSTIC-FIBROSIS GENE ; NF-KAPPA-B ; BREAST-CANCER ; PANCREATIC ADENOCARCINOMA ; HEPATOCELLULAR-CARCINOMA ; MESENCHYMAL TRANSITION ; MUC4 EXPRESSION ; CELL MIGRATION ; MIR-200 FAMILY
英文摘要

Cystic fibrosis (CF) transmembrane conductance regulator (CFTR) is expressed in the epithelial cells of a wide range of organs/tissues from which most cancers are derived. Although accumulating reports have indicated the association of cancer incidence with genetic variations in CFTR gene, the exact role of CFTR in cancer development and the possible underlying mechanism have not been elucidated. Here, we report that CFTR expression is significantly decreased in both prostate cancer cell lines and human prostate cancer tissue samples. Overexpression of CFTR in prostate cancer cell lines suppresses tumor progression (cell growth, adhesion and migration), whereas knockdown of CFTR leads to enhanced malignancies both in vitro and in vivo. In addition, we demonstrate that CFTR knockdown-enhanced cell proliferation, cell invasion and migration are significantly reversed by antibodies against either urokinase plasminogen activator (uPA) or uPA receptor (uPAR), which are known to be involved in various malignant traits of cancer development. More interestingly, overexpression of CFTR suppresses uPA by upregulating the recently described tumor suppressor microRNA-193b (miR-193b), and overexpression of pre-miR-193b significantly reverses CFTR knockdown-enhanced malignant phenotype and abrogates elevated uPA activity in prostate cancer cell line. Finally, we show that CFTR gene transfer results in significant tumor repression in prostate cancer xenografts in vivo. Taken together, the present study has demonstrated a previously undefined tumor-suppressing role of CFTR and its involvement in regulation of miR-193b in prostate cancer development.

语种英语
所属项目编号2012CB944900 ; GRF-CUHK466111
资助者Focused Investment Scheme of the Chinese University of Hong Kong and National 973 project ; Fundamental Research Funds for the Central Universities (JiNan University) ; Focused Investment Scheme of the Chinese University of Hong Kong and National 973 project ; Fundamental Research Funds for the Central Universities (JiNan University)
WOS记录号WOS:000318683600005
引用统计
被引频次:41[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/400002259/53546
专题北京大学深圳医院
作者单位1.Chinese Univ Hong Kong, Sch Biomed Sci, Epithelial Cell Biol Res Ctr, Shatin, Hong Kong, Peoples R China
2.Chinese Univ Hong Kong, Minist Educ Peoples Republ China, Key Lab Regenerat Med, Jinan Univ, Guangzhou, Guangdong, Peoples R China
3.Cardiff Univ, Sch Med, Metastasis & Angiogenesis Res Grp, Dept Surg, Cardiff CF10 3AX, S Glam, Wales
4.Peking Univ, Shenzhen Hosp, Shenzhen Key Lab Male Reprod Med & Genet, Shenzhen, Peoples R China
5.Chinese Univ Hong Kong, Fac Med, Dept Med & Therapeut, Li Ka Shing Inst Hlth Sci, Shatin, Hong Kong, Peoples R China
6.Chinese Univ Hong Kong, Div Urol, Dept Surg, Shatin, Hong Kong, Peoples R China
7.Chinese Univ Hong Kong, Prince Wales Hosp, Dept Anat & Cellular Pathol, Shatin, Hong Kong, Peoples R China
8.Sichuan Univ, Chinese Univ Hong Kong, West China Second Univ Hosp, Joint Lab Reprod Med, Chengdu 610064, Peoples R China
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Xie, C.,Jiang, X. H.,Zhang, J. T.,et al. CFTR suppresses tumor progression through miR-193b targeting urokinase plasminogen activator (uPA) in prostate cancer[J]. ONCOGENE,2013,32(18):2282-2291.
APA Xie, C..,Jiang, X. H..,Zhang, J. T..,Sun, T. T..,Dong, J. D..,...&Chan, H. C..(2013).CFTR suppresses tumor progression through miR-193b targeting urokinase plasminogen activator (uPA) in prostate cancer.ONCOGENE,32(18),2282-2291.
MLA Xie, C.,et al."CFTR suppresses tumor progression through miR-193b targeting urokinase plasminogen activator (uPA) in prostate cancer".ONCOGENE 32.18(2013):2282-2291.
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