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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; Byoung-Mog Kwon
- Bibliographic Citation
- Journal of Biological Chemistry, vol. 279, no. 8, pp. 6911-6920
- Publication Year
- 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.
- Amer Soc Biochemistry Molecular Biology Inc
- Appears in Collections:
- Division of Biomedical Research > Personalized Genomic Medicine Research Center > 1. Journal Articles
Division of Biomaterials Research > Industrial Bio-materials Research Center > 1. Journal Articles
Ochang Branch Institute > Division of Bioinfrastructure > 1. Journal Articles
Division of Biomedical Research > Genome Editing Research Center > 1. Journal Articles
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