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Barbigerone, a Natural Isoflavone, Induces Apoptosis in Murine Lung-Cancer Cells via the Mitochondrial Apoptotic Pathway
Author(s) -
Zhengguang Li,
Yinglan Zhao,
Xiaohua Wu,
Hao-Yu Ye,
Aihua Peng,
Zhixing Cao,
Yong-Qiu Mao,
Yuzhu Zheng,
Peidu Jiang,
Xia Zhao,
Lijuan Chen,
Yuquan Wei
Publication year - 2009
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000227817
Subject(s) - apoptosis , protein kinase b , mapk/erk pathway , cancer cell , cytochrome c , microbiology and biotechnology , downregulation and upregulation , biology , protein kinase a , cancer research , cell growth , programmed cell death , kinase , chemistry , cancer , biochemistry , genetics , gene
Barbigerone is a naturally occurring isoflavone with antioxidant activity. In present study, we investigated the antitumor activity of barbigerone against murine lung cancer cells LL/2 and the possible mechanism in vitro. Our results showed that barbigerone inhibited LL/2 cells proliferation in a concentration- and time-dependent manner and caused apoptotic death of LL/2 cells. Barbigerone-induced apoptosis was characterized by enhanced mitochondrial cytochrome c release, activation of caspase-3,-9, but not caspase-8. Exposure of LL/2 cells to barbigerone resulted in upregulation of Bcl-2-associated protein (Bax) and down-regulation of Bcl-2. In addition, proliferation inhibitory effect of barbigerone was associated with decreased level of phosphorylated p42/44 mitogen-activated protein kinase (p42/44 MAPK) and phosphorylated Akt. Moreover, barbigerone exhibit less toxicity to non-cancer cells than tumor cells. In conclusion, our results indicated that barbigerone can inhibit murine lung cancer cell proliferation by inducing apoptosis via mitochondrial apoptotic pathway and by decreasing phosphorylated p42/44 MAPK and Akt. Its potential to be a candidate of anti-cancer agent is worth being further investigated.

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