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Inhibition von ICE (Caspase-1) induziert Zelltod in Pankreaskarzinomzellen

Inhibition of ICE (caspase-1) induces cell death in pancreatic carcinoma cells

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Part of the book series: Deutsche Gesellschaft für Chirurgie ((FORUMBAND,volume 30))

Abstract

Background: In recent studies we demonstrated the overexpression of cysteine protease ICE (caspase-1) in pancreatic carcinoma tissue and the significant correlation with factors associated with poor prognosis, pointing to possible aspects of ICE in proliferative processes in human pancreatic carcinoma. In this study we investigated the influence of ICE inhibition on the cell cycle of pancreatic carcinoma cells. Methods: For cell cycle analysis and Western blot analysis, pancreatic cells (AsPC-1, BxPC-3, MiaPaCa-2 and Panc-1) were incubated with the specific ICE-inhibitor Ac-AAVALLPAVLLALLAP-YVAD.CHO (p-YVAD.CHO) for 24 h. Results: We found that incubation with p-YVAD.CHO (25 µM) induces a non-apoptotic/necrotic-like cell death in pancreatic AsPC-1 (24.5 ± 10.3%), BxPC-3 (21.9 ± 6.9%), MiaPaCa-2 (32.0 ± 16.2%) and Panc-1 (15.3 ± 1.1%) cells. Western blot analysis revealed an ICE-dependent modulation of the expression levels of the proteins of the bcl-2 family, known to play a key role in the regulation of cell death. Conclusion Our observations support our previous findings that ICE may be involved in antiapoptotic processes in pancreatic carcinoma and may provide new aspects in its role in proliferation and cell death.

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Correspondence to S. Schlosser .

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© 2001 Springer-Verlag Berlin Heidelberg

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Schlosser, S., Gansauge, F., Ramadani, M., Beger, H.G., Gansauge, S. (2001). Inhibition von ICE (Caspase-1) induziert Zelltod in Pankreaskarzinomzellen. In: Schönleben, K., Neugebauer, E., Hartel, W., Menger, M.D. (eds) Chirurgisches Forum 2001 für experimentelle und klinische Forschung. Deutsche Gesellschaft für Chirurgie, vol 30. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-56698-1_8

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  • DOI: https://doi.org/10.1007/978-3-642-56698-1_8

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-540-41718-7

  • Online ISBN: 978-3-642-56698-1

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