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Tetraoxyethylene isooctylphenyl ether(Militarin‐5) induces apoptosis in A549 cells
Author(s) -
Kim TaeWoong,
Lim MiHee,
Lim DongUk,
Yoon DeokHyo,
Cho JaeYoul,
Park Haeil,
Sung JaeMo,
Hwang KiChul
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.533.2
Subject(s) - apoptosis , a549 cell , poly adp ribose polymerase , cordyceps militaris , mtt assay , microbiology and biotechnology , dna fragmentation , chemistry , programmed cell death , western blot , propidium iodide , fragmentation (computing) , cytochrome c , flow cytometry , biology , biochemistry , dna , ecology , food science , cordyceps , polymerase , gene
Tetraoxyethylene isooctylphenyl ether(Militarin‐5) is one of the derivatives of Militarin, which is found from Cordyceps militaris . Cordyceps militaris is a parasitic fungus and has long been used as a Chinese medicine to treat illnesses, promote longevity, increase athletic power, and relieve exhaustion and anticancer. In this study, Militarin‐5 was synthesized, and, especially, we focused on the mechanisms of cell death exhibited by Militarin‐5 against human lung adenocarcinoma epithelial cell line, A549. Militarin‐5 inhibited growth and induced apoptosis in A549 cells in a dose‐dependent manner as determined by MTT assay, DNA fragmentation and flow cytometry histograms by propidium iodine staining. In Western blot analysis, apoptosis in A549 cells was associated with the activation of caspase‐3, ‐9 and proteolytic cleavage of PARP, decrease of Bcl‐2/Bax protein ratio, and release of cytochrome C from mitochondria into cytosol. We also found that Militarin‐5 inhibited the expression of COX‐2 in A549 cells. These results show that apoptosis of Militarin‐5 toward A549 cells is mediated by mitochondria‐dependent death‐signaling pathway. Thus, it indicated that Militarin‐5 may be a potential candidate in future research and development of bioactive ingredients as anticancer agents. Supported by grant from KOTEF, Korea

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