Egr-1, a new downstream molecule of Epstein-Barr virus latent membrane protein 1

被引：18

作者：

Kim, Joo Hyun

Kim, Won Seog

Kang, Jung Hun

Lim, Ho-Yeong

Ko, Young-Hyeh

Park, Chaehwa

机构：

[1] Samsung Med Ctr, Biomed Res Inst, Seoul 135710, South Korea

[2] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Div Hematol Oncol, Seoul 135710, South Korea

[3] Gyeongsang Natl Univ Hosp, Dept Hematol Oncol, Jinju, South Korea

[4] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Pathol, Seoul 135710, South Korea

[5] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Ctr Canc, Seoul 135710, South Korea

来源：

FEBS LETTERS | 2007年 / 581卷 / 04期

关键词：

LMP1; Egr-1; Epstein-Barr virus; survival;

D O I：

10.1016/j.febslet.2007.01.020

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

To investigate the effect of Epstein-Barr virus (EBV) latent membrane protein 1 (LMP1) on human cancer cells, we sought to identify and analyze potential target genes that were differentially expressed in the presence and absence of LMP1. Our cDNA microarray analysis revealed that expression of early growth response gene-1 (Egr-1) was increased by LMP1 expression in MCF7 and Jurkat cells. An NF inhibitor (SN50) antagonized LMP1-induced enhancement of Egr-1 expression, indicating that LMP1 induced Egr-1 via NF kappa B. Furthermore, three lines of evidence indicated that Egr-1 was required for LMP1-induced cancer cell survival. First, Egr-1 expression enhanced the survival of doxorubicin-treated MCF7 cells. Second, inhibition of Egr-1 expression by siRNA (siEgr-1) effectively suppressed LMP-1-induced survival of MCF7 cells. Third, Egr-1 knockdown decreased LMP1-induced expression of B111. Similar relationships among EBV infection, Egr-1 and drug resistance were also observed in tissues of peripheral T-cell lymphoma-unspecilied (PTCL-u) patients. (c) 2007 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

引用

页码：623 / 628

页数：6

共 33 条

[21] INHIBITION OF NUCLEAR TRANSLOCATION OF TRANSCRIPTION FACTOR NF-KAPPA-B BY A SYNTHETIC PEPTIDE-CONTAINING A CELL MEMBRANE-PERMEABLE MOTIF AND NUCLEAR-LOCALIZATION SEQUENCE [J].