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学科主题: 临床医学
题名:
PRL-3 activates NF-kappa B signaling pathway by interacting with RAP1
作者: Lian, Shenyi1; Meng, Lin1; Liu, Caiyun1; Xing, Xiaofang1; Song, Qian1; Dong, Bin2; Han, Yong1; Yang, Yongyong1; Peng, Lirong3; Qu, Like1; Shou, Chengchao1
关键词: PRL-3 ; RAP1 ; NF-kappa B ; Cancer
刊名: BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
发表日期: 2013-01-04
DOI: 10.1016/j.bbrc.2012.11.036
卷: 430, 期:1, 页:196-201
收录类别: SCI
文章类型: Article
WOS标题词: Science &a !E
类目[WOS]: Biochemistry & Molecular Biology ; Biophysics
研究领域[WOS]: Biochemistry & Molecular Biology ; Biophysics
关键词[WOS]: GENE-EXPRESSION ; TYROSINE PHOSPHATASES ; COLORECTAL-CANCER ; PROTEIN COMPLEX ; METASTASIS ; INVASION ; OVEREXPRESSION ; INFLAMMATION ; INHIBITION ; MIGRATION
英文摘要:

Phosphatase of regenerating liver (PRL-3) promotes cancer metastasis through enhanced cell motility and invasiveness, however its role in tumorigenesis remains unclear. Herein, we reported that PRL-3 interacts with telomere-related protein RAP1. PRL-3 promotes the cytosolic localization of RAP1, which is counteracted by silencing of PRL-3. Immunohistochemical staining of colon cancer tissue array (n = 170) revealed that high level of PRL-3 associates with cytosolic localization of RAP1 (p = 0.01). Microarray analysis showed that PRL-3 regulates expression of diverse genes and enhances phosphorylation of p65 subunit of NF-kappa B in a RAP1-dependent manner. Furthermore, PRL-3 transcriptionally activates RAP1 expression, which is counteracted by ablating p65. Therefore, our results demonstrate PRL-3 as a novel regulator of NF-kappa B signaling pathway through RAP1. (C) 2012 Elsevier Inc. All rights reserved.

语种: 英语
所属项目编号: 2009CB521805 ; 81230046 ; 30973407
项目资助者: National 973 Program of China ; National Natural Science Foundation of China
WOS记录号: WOS:000314320700034
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/54452
Appears in Collections:北京大学临床肿瘤学院_病理科_期刊论文

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作者单位: 1.Peking Univ, Canc Hosp & Inst, Dept Biochem & Mol Biol, Key Lab Carcinogenesis & Translat Res,Minist Educ, Beijing 100142, Peoples R China
2.Peking Univ, Canc Hosp & Inst, Dept Pathol, Key Lab Carcinogenesis & Translat Res,Minist Educ, Beijing 100142, Peoples R China
3.Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Dept Mol Oncol, Tampa, FL 33612 USA

Recommended Citation:
Lian, Shenyi,Meng, Lin,Liu, Caiyun,et al. PRL-3 activates NF-kappa B signaling pathway by interacting with RAP1[J]. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS,2013,430(1):196-201.
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