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Blood, 1 June 2001, Vol. 97, No. 11, pp. 3596-3604
NEOPLASIA
CD99 expression is positively regulated by
Sp1 and is negatively regulated by Epstein-Barr virus
latent membrane protein 1 through nuclear
factor- B
Im-soon Lee,
Min Kyung Kim,
Eun Young Choi,
Anja Mehl,
Kyeong Cheon Jung,
Min Chan Gil,
Martin Rowe, and
Seong Hoe Park
From the Department of Pathology and the Research
Division of Human Life Science, Seoul National University College of
Medicine; the Department of Pathology, Hallym University College of
Medicine, Chunchon; DiNonA Inc, Suwon, Korea; and the
Department of Medicine, University of Wales College of Medicine,
Cardiff, United Kingdom.
Epstein-Barr virus (EBV)-encoded latent membrane protein-1 (LMP1)
is highly expressed in Hodgkin and Reed-Sternberg (H-RS) cells from
patients with EBV-associated Hodgkin disease. It was previously
demonstrated that CD99 can be negatively regulated by LMP1 at the
transcriptional level, and the decreased expression of CD99 in a B
lymphocyte cell line generates H-RS-like cells. In this study,
detailed dissection of the CD99 promoter region was performed to search
regulatory factor(s) involved in the expression of the gene. Using
various mutant constructs containing deletions in the promoter region,
it was revealed that the maximal promoter activity was retained on
5'-deletion to the position  137 from the transcriptional initiation
site. Despite the presence of multiple putative Sp1-binding sites in
the promoter region, the site located at 95 contributes heavily as a
positive cis-acting element to its basal promoter activity.
However, on examination of the involvement of the positive-acting
Sp1-binding site of the promoter for the repressive activity of LMP1,
it appeared to be dispensable. Instead, the repressive effect was
mapped to the nuclear factor (NF)- B activation domains in the
cytoplasmic carboxyl terminus of LMP1 despite the absence of the
NF-B consensus sequences in the CD99 promoter region. Furthermore,
the decreased CD99 promoter activity by LMP1 was markedly restored when
NF-B activity was inhibited. Taken together, these data suggest that
Sp1 activates, whereas LMP1 represses, transcription from the CD99
promoter through the NF-B signaling pathway, and they might aid
in the understanding of the molecular mechanisms of viral
pathogenesis in EBV-positive Hodgkin disease.
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