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Carcinogenesis Advance Access originally published online on April 18, 2006
Carcinogenesis 2006 27(10):1991-2000; doi:10.1093/carcin/bgl046
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© The Author 2006. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Hypericum sampsonii induces apoptosis and nuclear export of retinoid X receptor-alpha

Jin-Zhang Zeng1,*,{dagger}, De-Fu Sun1,{dagger}, Li Wang1, Xihua Cao3, Jian-Bin Qi2, Ting Yang1, Chang-Qi Hu2, Wen Liu3 and Xiao-Kun Zhang1,3

1 Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences Shanghai, China
2 School of Pharmacy, Medical Center of Fudan University Shanghai, China
3 Cancer Center, Burnham Institute for Medical Research La Jolla, CA, USA

*To whom correspondence should be addressed at: The Samost Center, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 500 Caobao Road, Shanghai 200233, China. Tel: +86 21 54481877; Fax: +86 21 54971085; Email: jzzeng{at}sibs.ac.cn

Natural products derived from plants provide a rich source for development of new anticancer drugs. Recent studies suggest that modulation of subcellular localization of retinoid X receptor-alpha (RXR{alpha}) represents a potential approach for inducing cancer cell apoptosis. In this study, we screened a herbal library for inducing translocation of RXR{alpha} from the nucleus to the cytoplasm. Our results revealed that the extract of Hypericum sampsonii, a member of the genus Hypericum, had remarkable effect on RXR{alpha} subcellular localization in various cancer cells. Treatment of NIH-H460 human lung cancer cells with H.sampsonii extract resulted in relocalization of RXR{alpha} from the nucleus to the cytoplasm. Cytoplasmic RXR{alpha} induced by H.sampsonii was associated with mitochondria, accompanied with cytochrome c release and apoptosis. H.sampsonii extract effectively inhibited the growth of various cancer cell lines, including NIH-H460 lung cancer, MGC-803 stomach cancer and SMMC7721 liver cancer cells. The growth inhibitory effect of H.sampsonii extract depended on levels of RXR{alpha}, as it failed to inhibit the growth of CV-1 cells lacking detectable RXR{alpha}, whereas transfection of RXR{alpha} into CV-1 cells restored its apoptotic response to H.sampsonii. Furthermore, the apoptotic effect of H.sampsonii was significantly enhanced when RXR{alpha} was overexpressed in NIH-H460 cells. Together, our results demonstrate that H.sampsonii contains ingredient(s) that induce apoptosis of cancer cells by modulating subcellular localization of RXR{alpha}.


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