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Journal of Biomedicine and Biotechnology
Volume 2011 (2011), Article ID 636497, 9 pages
Research Article

Transcription Factor Sp1 Is Involved in Expressional Regulation of Coxsackie and Adenovirus Receptor in Cancer Cells

1Division of Intractable Diseases, Center for Biomedical Sciences, National Institute of Health, Osong Health Technology Administration Complex, 187 Osongsaengmyeo2(i)-ro, Gangoemyeon, Cheongwon-gun, Chungcheongbuk-do 363-951, Republic of Korea
2Section of Molecular Biology, Division of Biological Sciences, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0322, USA
3School of Life Sciences and Biotechnology, Korea University, Seoul 136-701, Republic of Korea
4Department of Biotechnology, The Catholic University of Korea, 43-1 Yeokgok 2-dong, Wonmi-gu, Gyeonggi-do, Bucheon 420-743, Republic of Korea

Received 18 July 2011; Revised 17 September 2011; Accepted 7 October 2011

Academic Editor: Decheng Yang

Copyright © 2011 Sun-Ku Chung et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Coxsackie and adenovirus receptor (CAR) was first known as a virus receptor. Recently, it is also known to have tumor suppressive activity such as inhibition of cell proliferation, migration, and invasion. It is important to understand how CAR expression can be regulated in cancers. Based on an existence of putative Sp1 binding site within CAR promoter, we investigated whether indeed Sp1 is involved in the regulation of CAR expression. We observed that deletion or mutation of Sp1 binding motif (−503/−498) prominently impaired the Sp1 binding affinity and activity of CAR promoter. Histone deacetylase inhibitor (TSA) treatment enhanced recruitment of Sp1 to the CAR promoter in ChIP assay. Meanwhile, Sp1 binding inhibitor suppressed the recruitment. Exogenous expression of wild-type Sp1 increased CAR expression in CAR-negative cells; meanwhile, dominant negative Sp1 decreased the CAR expression in CAR-positive cells. These results indicate that Sp1 is involved in regulation of CAR expression.