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J. Biol. Chem., Vol. 279, Issue 8, 6911-6920, February 20, 2004

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2'-Benzoyloxycinnamaldehyde Induces Apoptosis in Human Carcinoma via Reactive Oxygen Species^*

Dong Cho Han, Mi-Young Lee, Ki Deok Shin, Sun Bok Jeon, Jung Min Kim, Kwang-Hee Son, Hyoung-Chin Kim, Hwan-Mook Kim, and Byoung-Mog Kwon

From the Korea Research Institute of Bioscience and Biotechnology, 52 Uendong Yoosunggu, Taejeon 305-600, Korea

2'-Hydroxycinnamaldehyde (HCA) has been shown to have inhibitory effects on farnesyl protein transferase in vitro, angiogenesis, and tumor cell growth. However, mechanism for these inhibitions remains unknown. As a derivative of HCA, BCA (2'-benzoyl-oxycinnamaldehyde) was synthesized by replacing hydroxyl group with benzoyl-oxyl group. When p53-mutated cancer cell lines (MDA-MB-231 breast cancer cell and SW620 colon cancer cell) were treated with 10 µM HCA or BCA, it induced growth arrest and apoptosis of tumor cells. Markers of apoptosis such as degradations of chromosomal DNA and poly(ADP-ribose) polymerase and activation of caspase-3 were detected after HCA or BCA treatment. BCA-induced apoptosis was blocked by pretreatment of cells with anti-oxidants, glutathione, or N-acetyl-cysteine. In addition, BCA-induced activation of caspase-3 and degradation of poly(ADP-ribose) polymerase were abolished by pretreatment of cells with the anti-oxidants. These results suggest that reactive oxygen species are major regulator of BCA-induced apoptosis. HCA or BCA-induced accumulation of reactive oxygen species was detected by using DCF-DA, an intracellular probe of oxidative stress. Furthermore, when BCA (100 mg/kg) was administrated intraperitoneally or orally into a nude mouse, it inhibited >88 or 41% of tumor growth, respectively, without any detectable weight change. These results suggest that BCA is a good drug candidate for cancer therapy.

Received for publication, September 2, 2003 , and in revised form, November 11, 2003.

^* This work was supported by Plant Diversity Research Center (PF0320506-0) and the Center for Biological Modulators (CBM1-B500-001-1-0-0) of the 21^st Century Frontier Research Program, the Good Health R&D Program (01-PJ2-PG4-J201PT01-008), and the KRIBB Research Initiative Program. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

To whom correspondence should be addressed. Tel.: 82-42-860-4557; Fax: 82-42-861-2675; E-mail: kwonbm{at}kribb.re.kr.

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