Carcinogenesis Advance Access published online on December 12, 2005
Carcinogenesis, doi:10.1093/carcin/bgi306
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1 Beijing Genomics Institute, Chinese Academy of Sciences, Beijing Airport Industrial Zone B-6, Shunyi, Beijing 101300, China; Beijing Proteomics Institute, Beijing Airport Industrial Zone B-6, Shunyi, Beijing 101300, China; Graduate School of Chinese Academy of Sciences, Beijing 100049, China
* To whom correspondence should be addressed. Garlic is generally used as a therapeutic reagent against various diseases worldwide. Although a great effort is made to understand the pharmaceutical mechanisms of garlic and its derivatives, there are many mysteries to be uncovered. Using proteomic means, herein we have systematically studied the responses of protein expression in BGC823 cells, a gastric cancer cell line, induced by diallyl trisulfide (DATS), a major component of garlic derivatives. A total of 41 unique proteins in BGC823 were detected significant changes in their expression levels corresponding with DATS administration. Of these proteins, five typical ones, GST-pi, VDAC-1, Annexin I, Galectin, and S100A11, were further examined by Western blotting, resulting in the coincident data with the proteomic evidence. Moreover the quantitative real-time RT-PCR experiments offered the dynamic data of mRNA expression, indicating the responses of Annexin I and GST-pi expression within a short period after DATS treatment. Interestingly, almost 50% of DATS-sensitive proteins (19/41) in BGC823 are tightly associated with apoptotic pathways. These proteomic results presented, therefore, provide additional support to the hypothesis that garlic is a stronger inducer of apoptosis in tumor cells.
Received August 18, 2005
Revised September 30, 2005
Accepted December 6, 2005
MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION
A proteomic investigation into a human gastric cancer cell line BGC823 treated with diallyl trisulfide
Na Li 1
,
Ruifang Guo 2
,
Wenmei Li 2,
Jianmin Shao 3,
Shuting Li 3,
Kang Zhao 3,
Xishu Chen 3,
Ningzhi Xu 3,
Siqi Liu 3,
and
Youyong Lu 4 *
2 Peking University School of Oncology & Beijing Institute for Cancer Research, Beijing 100034, China
3 Beijing Genomics Institute, Chinese Academy of Sciences, Beijing Airport Industrial Zone B-6, Shunyi, Beijing 101300, China; Beijing Proteomics Institute, Beijing Airport Industrial Zone B-6, Shunyi, Beijing 101300, China
4 Beijing Genomics Institute, Chinese Academy of Sciences, Beijing Airport Industrial Zone B-6, Shunyi, Beijing 101300, China; Beijing Proteomics Institute, Beijing Airport Industrial Zone B-6, Shunyi, Beijing 101300, China; Peking University School of Oncology & Beijing Institute for Cancer Research, Beijing 100034, China
Youyong Lu, E-mail: yongylu{at}public.bta.net.cn
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Abstract
These authors contributed equally.
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