Korean J Phys Anthropol.
2007 Sep;20(3):245-255.
Translocation of Phospho-ser 15-p53 in Eugenol-induced Apoptosis of in vitro Cultured Cancer Cells
- Affiliations
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- 1Department of Oral Anatomy, College of Dentistry, Pusan National University. parkbs@pusan.ac.kr
- 2Department of Biology, College of Natural Science, Pusan National University.
- 3Department of Anatomy, College of Medicine, Dong-A University.
Abstract
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Eugenol (4-allyl-2-methoxyphenol), a major ingredient of herbs such as clove and Magnoliae Flos, is known to induce apoptosis in mast cells via p53 pathway. This study was undertaken to examine the in vivo effect of eugenol and the molecular mechanism underlying eugenol-induced apoptosis in several cancer cells with different p53 status. Effect of eugenol on mesenteric mast cells was tested using a rat anaphylaxis model. And TUNEL staining was conducted to observe the cells undergoing apoptosis. Several cancer cells were treated with eugenol, and Western blotting, immunocytochemistry, confocal microscopy and mitochondrial fractionation were conducted. Eugenol induced apoptosis in mast cells of mesentery in vivo, decreasing the density of mast cells. Although eugenol did not increase the expression level of p53, it caused the translocation of p53 into mitochondria and subsequent release of cytochrome c. Eugenol increased the level of phospho-ser 15-p53 in several cancer cells with wild type p53 but not in the cells with mutant p53 or p53 deficient cancer cell. In cancer cells with wild type p53, p53 translocated into mitochondria was phosphorylated on ser 15. In conclusion, eugenol induces apoptosis in cancer cells with wild type p53 via the translocation of phospho-ser 15- p53. Furthermore our data suggest that the anticancer effect on cancer cells with wild type p53 may be involved with the pharmacological effect of eugenol regulating apoptosis via a phospho-ser 15-p53 dependent fashion.