Abstract:
:Chemokines and chemokine receptors mediate lymphocyte migration and tissue localization. To analyze CCL5 (RANTES) expression by EBV-infected cells, we examined the expression of CCL5 in BL cell lines. Among 4 BL cell lines, those infected with EBV selectively expressed the CCL5 gene and secreted CCL5. Four cell lines also expressed CCR5, a receptor for CCL5. EBV-encoded LMP-1, a pleiotropic protein that effects gene expression, cell transformation, growth and death, induces expression of CCL5 mRNA and secretion of CCL5 in the EBV-negative BL cell line BJAB and the embryonic kidney cell line 293T. HDACI-stimulated endogenous LMP-1 also induced CCL5 expression in an EBV-positive BL cell line. Analysis of the CCL5 promoter revealed that it is activated by both LMP-1 C-terminal activation domains, CTAR-1 and CTAR-2, which can activate NF-kappaB signaling. Coexpression of IkappaBalpha, IkappaBbeta, IKKalpha, IKKbeta, NIK and TRAF2 dominant-negative constructs, with LMP-1 inhibited the activation of the CCL5 promoter by LMP-1, suggesting that LMP-1 induces CCL5 via NF-kappaB signaling. The NF-kappaB binding sites, R(A/B), located at positions -71 to -43 relative to the putative transcription start site in the CCL5 promoter, were essential for the activation of CCL5 gene expression by LMP-1. These results indicate that the activation of the NF-kappaB pathway by LMP-1 is required for the activation of CCL5 expression.
journal_name
Int J Cancerjournal_title
International journal of cancerauthors
Uchihara JN,Krensky AM,Matsuda T,Kawakami H,Okudaira T,Masuda M,Ohta T,Takasu N,Mori Ndoi
10.1002/ijc.20784keywords:
subject
Has Abstractpub_date
2005-05-01 00:00:00pages
747-55issue
5eissn
0020-7136issn
1097-0215journal_volume
114pub_type
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