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Millitarin‐1(M1), a synthesized isooctylphenyl derivative induced mitochondrial dependent apoptosis and ROS generation in A549 Cells
Author(s) -
Kim Tae-Woong,
Lim Mi-Hee,
Yoon Deok-Hyo,
Park Haeil,
Cho Jae-Youl,
Sung Gi-Ho,
Lee Tae-Ho
Publication year - 2012
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.26.1_supplement.lb178
Subject(s) - apoptosis , a549 cell , reactive oxygen species , microbiology and biotechnology , p38 mitogen activated protein kinases , chemistry , cell growth , cell cycle , cell cycle checkpoint , cytochrome c , kinase , biology , biochemistry , mapk/erk pathway
Millitarin‐1(M1), a synthesized isooctylphenyl derivative on the basis of millitarin, which is found from Cordyceps millitaris. Cordyceps millitaris 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. M1 suppresses effectively proliferation of A549, human lung adenocarcinoma, by causing apoptosis. M‐1 triggered the mitochondrial apoptotic pathway, as indicated by a change in proapoptotic moleculas(Bax, Bak, Bim)/ant‐apoptotic molecules(Bcl‐2, Bcl‐xL) ratios, resulting in cytochrome c release, and caspase‐3 and 9 activation. We also found that the generation of reactive oxygen species(ROS) is a critical mediator in the inhibition of M1 induced cell growth of A549. We observed that M1 treatment significantly inhibited cell growth in a concentration dependent manner and caused sub G0/G1 phase cell cycle arrest. Enhancement of ROS by M1 activated apoptosis and resulted in the increased activation of c‐Jun NH2‐terminal kinase, p38 and ERK1/2. Therefore, it indicated that M1 may be a potential candidate in future research and development of bioactive ingredients as anticancer agents. Supported by a grant from RDA(No. PJ008321), Korea