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Originally published In Press as doi:10.1074/jbc.M203706200 on May 17, 2002

J. Biol. Chem., Vol. 277, Issue 31, 27748-27756, August 2, 2002
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Human Papillomavirus E2 Down-regulates the Human Telomerase Reverse Transcriptase Promoter*

Daeyoup LeeDagger §, Hak-Zoo KimDagger §, Kwi Wan JeongDagger , Young Sam ShimDagger , Izumi Horikawa, J. Carl Barrett, and Joonho ChoeDagger ||

From the Dagger  Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon 305-701, Korea and the  Laboratory of Biosystems and Cancer, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892

The transcriptional regulation of the human telomerase reverse transcriptase (hTERT) gene is a critical step in transformation and differentiation. Human papillomavirus E2 protein inhibits cell growth in HPV-infected cells and triggers apoptosis in HeLa cells. Because E2 induces cell growth suppression and senescence, we hypothesize that the protein may modulate cellular gene expression related to these processes. In this report, we demonstrate that E2 inhibits the hTERT promoter. The mapping of the E2-responsive region of hTERT reveals that Sp1 is important for E2-mediated repression of this promoter in 293T cells. Site-directed mutagenesis data on the hTERT promoter show that E2 does not abolish E-Box-mediated transcription and represses promoter activity via the Sp1 binding site. Furthermore, chromatin immunoprecipitation assays indicate that E2 is actively recruited to the hTERT promoter region. Our findings provide novel insights into the biological function of human papillomavirus E2.

* This work was supported in part by the National Research Laboratory Program of the Korea Institute of Science & Technology Evaluation and Planning (KISTEP), the Molecular Medicine Research Program of KISTEP through the Biomedical Research Center at Korea Advanced Institute of Science and Technology, and the Korea Science and Engineering Foundation through the Protein Network Research Center at Yonsei University.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ Both authors contributed equally to this work.

|| To whom correspondence should be addressed. Tel.: 82-42-869-2630; Fax: 82-42-869-5630; E-mail: jchoe@mail.kaist.ac.kr.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.


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