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Journal of OncologyVolume 2008 2008, Article ID 285374, 5 pages

Research Article

Medical School, Hanyang University, Seoul 133-791, South Korea

Department of Research and Development, HanCell Inc, Incheon 406-799, South Korea

Department of Biomedical Science, National Institute of Health, Seoul 122-701, South Korea

Department of Biological Science, Gachon University of Medicine and Science, Incheon 406-799, South Korea

Received 9 June 2008; Revised 17 July 2008; Accepted 22 July 2008

Academic Editor: Krešimir Pavelić

Copyright © 2008 Sang Koo Lee 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.


Aspirin and other nonsteroidal anti-inflammatory drugs show efficacy in the prevention of cancers. It is known that they can inhibit cyclooxygenases, and some studies have shown that they can induce apoptosis. Our objective in this study was to investigate the mechanism by which aspirin exerts its apoptosis effects in human cervical cancer HeLa cells. The effect of aspirin on the gene expression was studied by differential mRNA display RT-PCR. Among the isolated genes, mu-type calpain gene was upregulated by aspirin treatment. To examine whether calpain mediates the antitumor effects, HeLa cells were stably transfected with the mammalian expression vector pCR3.1 containing mu-type calpain cDNA pCRCAL-HeLa, and tumor formations were measured in nude mice. When tumor burden was measured by day 49, HeLa cells and pCR-HeLa cells vector control produced tumors of 2126  and 1638  , respectively, while pCRCAL-HeLa cells produced markedly smaller tumor of 434  in volume. The caspase-3 activity was markedly elevated in pCRCAL-HeLa cells. The increased activity levels of caspase-3 in pCRCAL-HeLa cells, in parallel with the decreased tumor formation, suggest a correlation between caspase-3 activity and calpain protein. Therefore, we conclude that aspirin-induced calpain mediates an antitumor effect via caspase-3 in cervical cancer cells.

Author: Sang Koo Lee, Min Seon Park, and Myeong Jin Nam



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