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Carcinogenesis Advance Access originally published online on December 19, 2005
Carcinogenesis 2006 27(5):936-944; doi:10.1093/carcin/bgi316
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© The Author 2005. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Overexpression of thymosin ß-4 renders SW480 colon carcinoma cells more resistant to apoptosis triggered by FasL and two topoisomerase II inhibitors via downregulating Fas and upregulating Survivin expression, respectively

Hung-Liang Hsiao, Wei-Shu Wang 1, Po-Min Chen 1 and Yeu Su 2, *

Institute of Pharmacology, College of Medicine, National Yang-Ming University, Shih-Pai, Taipei 11221, Taiwan, R.O.China, 1 Division of Medical Oncology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan, R.O.China and 2 Institute of Biopharmaceutical Science, Collage of Life Science, National Yang-Ming University, Taipei, Taiwan, R.O.China

* To whom correspondence should be addressed. Email: yeusu{at}ym.edu.tw

The present work was conducted to further examine the effects of thymosin ß-4 (Tß4) upregulation on the apoptosis of SW480 colon cancer cells induced by T cells and various chemotherapeutic agents because reduced susceptibility to the cytotoxicity of an anti-Fas IgM (CH-11) in Tß4-overexpressing cells has previously been reported by us. As expected, Tß4 overexpressers were also more resistant to the killing effect of FasL-bearing Jurkat T cells. On the other hand, pretreating these cells with an MMP inhibitor restored not only their Fas levels but also their sensitivity to CH-11, suggesting a pivotal role of MMP in downregulating Fas in Tß4 overexpressers. Interestingly, while the susceptibilities of Tß4 overexpressers to 5-FU and irinotecan remained unchanged, they were more resistant to doxorubicin and etoposide which triggered apoptosis via a mitochondrial pathway. Concordantly, activation of both caspases 9 and 3 in Tß4 overexpressers by the two aforementioned topoisomerase II inhibitors was dramatically abrogated which could be accounted mainly by an increased expression of Survivin, a critical anti-apoptotic factor. Finally, poor survival was found in stage III colon cancer patients whose tumors were stained positively by the anti-Survivin antibody. Thus, advantages such as immune evasion and resistance to anticancer drug-induced apoptosis acquired by colon cancer cells through Tß4 overexpression might facilitate their survival during metastasis and chemotherapy.


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