Abstract |
In this study, we investigated the effects of 2,3,6-tribromo-4,5-dihydroxybenzyl methyl ether (TDB), isolated from Symphyocladia latiuscula (marine red algae), on the proliferation of MCF-7 human breast cancer cells. TDB treatment for 48 h inhibited cancer cell growth and induced DNA fragmentation. Furthermore, morphological characterizations such as apoptotic bodies and membrane blebs were shown by electronic microscopy. TDB-induced apoptosis in the MCF-7 cells was closely linked with the down-regulation of Bcl-2 protein expression and the cleavage of caspase-3 substrates, with poly(ADP-ribose) polymerase cleavage occurring by TDB treatment. TDB treatment also caused a marked increase in the level of p21WAF1/CIP1 protein in a p53-dependent manner. In addition, the upregulation of p21WAF1/CIP1 in the MCF-7 cells was related to a decrease in c-Myc protein in a dose-dependent manner. Based on our data, TDB is a good candidate for further evaluation as an effective chemotherapeutic agent, acting through the induction of apoptosis.
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Authors | Ji-Hyeon Lee, Sang Eun Park, Mohammad Akbar Hossain, Min Young Kim, Mi-Na Kim, Hae Young Chung, Jae Sue Choi, Young Hyun Yoo, Nam Deuk Kim |
Journal | Archives of pharmacal research
(Arch Pharm Res)
Vol. 30
Issue 9
Pg. 1132-7
(Sep 2007)
ISSN: 0253-6269 [Print] Korea (South) |
PMID | 17958331
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- 2,3,6-tribromo-4,5-dihydroxybenzyl methyl ether
- Antineoplastic Agents
- CDKN1A protein, human
- Cyclin-Dependent Kinase Inhibitor p21
- Ethers
- Proto-Oncogene Proteins c-bcl-2
- Proto-Oncogene Proteins c-jun
- Tumor Suppressor Protein p53
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Topics |
- Antineoplastic Agents
(pharmacology)
- Apoptosis
(drug effects)
- Breast Neoplasms
(drug therapy, pathology)
- Cell Line, Tumor
- Cell Proliferation
(drug effects)
- Cyclin-Dependent Kinase Inhibitor p21
(analysis)
- Ethers
(pharmacology)
- Female
- Humans
- Proto-Oncogene Proteins c-bcl-2
(analysis)
- Proto-Oncogene Proteins c-jun
(analysis)
- Tumor Suppressor Protein p53
(analysis, physiology)
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