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Ocimum sanctum induces apoptosis in A549 lung cancer cells and suppresses the in vivo growth of lewis lung carcinoma cells
Author(s) -
Magesh Venkataraman,
Lee JangChoon,
Ahn Kwang Seok,
Lee HyoJung,
Lee HyoJeong,
Lee EunOk,
Shim Bum Sang,
Jung Hee Jae,
Kim Jin Sung,
Kim Dae Keun,
Choi SeungHoon,
Ahn KyooSeok,
Kim SungHoon
Publication year - 2009
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.2784
Subject(s) - a549 cell , apoptosis , lewis lung carcinoma , protein kinase b , cancer research , biology , mapk/erk pathway , cytochrome c , in vivo , cancer cell , kinase , microbiology and biotechnology , chemistry , cancer , biochemistry , metastasis , genetics
Although Ocimum sanctum has been used extensively for its medicinal values in India and China, its antitumor activity against human nonsmall cell lung carcinoma (NSCLC) A549 cells has not been investigated until now. Therefore, the antitumor mechanism of ethanol extracts of Ocimum sanctum (EEOS) was elucidated in A549 cells in vitro and the Lewis lung carcinoma (LLC) animal model. EEOS exerted cytotoxicity against A549 cells, increased the sub‐G1 population and exhibited apoptotic bodies in A549 cells. Furthermore, EEOS cleaved poly(ADP‐ribose)polymerase (PARP), released cytochrome C into cytosol and simultaneously activated caspase‐9 and ‐3 proteins. Also, EEOS increased the ratio of proapoptotic protein Bax/antiapoptotic protein Bcl‐2 and inhibited the phosphorylation of Akt and extracellular signal regulated kinase (ERK) in A549 cancer cells. In addition, it was found that EEOS can suppress the growth of LLC inoculated onto C57BL/6 mice in a dose‐dependent manner. Overall, these results demonstrate that EEOS induces apoptosis in A549 cells via a mitochondria caspase dependent pathway and inhibits the in vivo growth of LLC, suggesting that EEOS can be applied to lung carcinoma as a chemopreventive candidate. Copyright © 2009 John Wiley & Sons, Ltd.