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Carcinogenesis Advance Access published online on December 3, 2004
Carcinogenesis, doi:10.1093/carcin/bgh345
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Oxford University Press
Received July 23, 2004
Revised November 11, 2004
Accepted November 21, 2004

CANCER BIOLOGY

Activation of caspase-8/Bid and Bax pathways in aspirin-induced apoptosis in gastric cancer

Qing Gu 1, Ji De Wang 2, Harry H. X. Xia 2, Marie C. M. Lin 3, Hua He 2, Bing Zou 2, Shui Ping Tu 2, Yi Yang 2, Xin Guang Liu 4, Shiu Kum Lam 2, Wai Man Wong 2, Annie O. O. Chan 2, Man Fung Yuen 2, Hsiang Fu Kung 3, and Benjamin Chun-Yu Wong 2*

1 Department of Gastroenterology, First Hospital, Peking University, Beijing, P.R. China; Department of Medicine, University of Hong Kong, Hong Kong
2 Department of Medicine, University of Hong Kong, Hong Kong
3 Institute of Molecular Biology, University of Hong Kong, Hong Kong
4 Department of Gastroenterology, First Hospital, Peking University, Beijing, P.R. China

* To whom correspondence should be addressed.
Benjamin Chun-Yu Wong, E-mail: bcywong{at}hku.hk


  Abstract

Aspirin-induced apoptosis is one of the important mechanisms for their anti-tumour effect in gastric cancer. We aimed at investigating the involvement of bcl-2 family members in the apoptotic pathway in gastric cancer. Gastric cancer cell line AGS and MKN-45 were observed as to cell growth inhibition and induction of apoptosis in response to treatment with aspirin. Cell proliferation was measured by MTT assay. Apoptosis was determined by DAPI staining. Protein expressions were determined by western blotting. We showed that aspirin activated caspase-8, caspase-9 and capase-3; cleaved and translocated Bid; induced conformational change and translocation of Bax and cytochrome c release. In addition, suppression of caspase-8 with specific inhibitor z-IETD-fmk, as well as pan-caspase inhibitor z-VAD-fmk, prevented Bid cleavage, and subsequent apoptosis. The caspase inhibitors failed to abolish effects on activation of Bax. In conclusion, our results identify the role of caspase-8/Bid and activation of Bax as a novel mechanism for aspirin-induced apoptosis in gastric cancer.


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