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Egr‐1, a new downstream molecule of Epstein‐Barr virus latent membrane protein 1
Author(s) -
Kim Joo Hyun,
Kim Won Seog,
Kang Jung Hun,
Lim Ho-Yeong,
Ko Young-Hyeh,
Park Chaehwa
Publication year - 2007
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2007.01.020
Subject(s) - jurkat cells , gene knockdown , cancer research , cell culture , biology , lymphoma , microbiology and biotechnology , virus , gene expression , cancer cell , microarray analysis techniques , microrna , gene , chemistry , cancer , virology , t cell , immunology , genetics , immune system
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 NFκB inhibitor (SN50) antagonized LMP1‐induced enhancement of Egr‐1 expression, indicating that LMP1 induced Egr‐1 via NFκB. 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 Bfl‐1. Similar relationships among EBV infection, Egr‐1 and drug resistance were also observed in tissues of peripheral T‐cell lymphoma‐unspecified (PTCL‐u) patients.