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http://dx.doi.org/10.5352/JLS.2009.19.4.502

Bee Venom-induced Growth Inhibition of Human Lung Cancer Cells was Associated with Inhibition of Prostagladin E2 Production and Telomerase Activity.  

Kim, Jong-Hwan (Departments of Internal Medicine, College of Oriental Medicine, Dong-Eui University)
Hwang, Won-Deuk (Departments of Internal Medicine, College of Oriental Medicine, Dong-Eui University)
Kim, Byung-Woo (Department of Biomaterial Control (BK21 program), Graduate School, Dong-Eui University)
Choi, Yung-Hyun (Departments of Biochemistry, College of Oriental Medicine, Dong-Eui University)
Publication Information
Journal of Life Science / v.19, no.4, 2009 , pp. 502-507 More about this Journal
Abstract
In modern oriental medicine, bee venom therapy is being used for aqua-acupuncture to relieve pain and to cure inflammatory diseases such as rheumatoid arthritis, osteoarthritis, and gout. Bee venom therapy has been processed and reported in many experimental studies, with regard to its effects on pain alleviation, anti-inflammation, removal of fever, anti-convulsion, suppression of tumor and immunity strengthening, etc., however, its mechanism of action, molecular targeting on prostaglandin $E_2$ ($PGE_2$) production and telomere length regulation in human cancer remains unclear. In this study, we investigated the effect of bee venom on the levels of cyclooxygenases (COXs) and telomere regulatory components of A549 human lung cancer cells. Bee venom-induced anti-proliferative effects of A549 cells were associated with the inhibition of human telomerase reverse transcriptase (hTERT) as well as human telomerase RNA (hTR), transcription factor c-myc and the activity of telomerase. In addition, bee venom treatment markedly decreased the levels of COX-2 mRNA and protein expression without significant changes in the expression of COX-1, which was correlated with a decrease in $PGE_2$ synthesis. Taken together, these findings provide important new insights into the possible molecular mechanisms of the anti-cancer activity of bee venom.
Keywords
Bee venom; prostaglandin $E_2$; telomerase;
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