Journal Article

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

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

in Carcinogenesis

Volume 26, issue 3, pages 541-546
Published in print March 2005 | ISSN: 0143-3334
Published online March 2005 | e-ISSN: 1460-2180 | DOI:
Activation of the caspase-8/Bid and Bax pathways in aspirin-induced apoptosis in gastric cancer

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  • Clinical Cytogenetics and Molecular Genetics


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Aspirin-induced apoptosis is one of the important mechanisms for its antitumour effect against 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 4′-6-diamidino-2-phenylindole staining. Protein expression was determined by western blotting. We showed that aspirin activated caspase-8, caspase-9 and capase-3, cleaved and translocated Bid, induced a conformational change in and translocation of Bax and cytochrome c release. In addition, suppression of caspase-8 with the specific inhibitor z-IETD-fmk, as well as the pan-caspase inhibitor z-VAD-fmk, prevented Bid cleavage and subsequent apoptosis. The caspase inhibitors failed to abolish the effects on Bax activation. In conclusion, our results identify a role of caspase-8/Bid and activation of Bax as a novel mechanism for aspirin-induced apoptosis in gastric cancer.

Keywords: DAPI, 4′-6-diamidino-2-phenylindole; GFP, green fluorescent protein; PARP, poly(ADP-ribose) polymerase; PBS, phosphate-buffered saline; tBid, truncated Bid; TNF, tumor necrosis factor

Journal Article.  3973 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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