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Tumour-cell apoptosis after cisplatin treatment is not telomere dependent

Lookup NU author(s): Jessie Jeyapalan, Dr Gabriele Saretzki, Alan Leake, Dr Michael Tilby, Professor Thomas von Zglinicki


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Cisplatin is a major chemotherapeutic agent, especially for the treatment of neuroblastoma. Telomeres with their sequence (TTAGGG)n are probable targets for cisplatin intrastrand cross-linking, but the role of telomeres in mediating cisplatin cytotoxicity is not clear. After exposure to cisplatin as single dose or continuous treatment, we found no loss of telomeres in either SHSY5Y neuroblastoma cells (telomere length, ∼4 kbp), HeLa 229 cells (telomere length, 20 kbp) or in the acute lymphoblastic T cell line 1301 (telomere length, ∼80 kbp). There was no induction of telomeric single strand breaks, telomeric overhangs were not degraded and telomerase activity was down-regulated only after massive onset of apoptosis. In contrast, cisplatin induced a delayed formation of DNA strand breaks and induced DNA damage foci containing γ-H2A.X at nontelomeric sites. Interstitial DNA damage appears to be more important than telomere loss or telomeric damage as induce r of the signal pathway towards apoptosis and/or growth arrest in cisplatin-treated tumour cells. © 2005 Wiley-Liss, Inc.

Publication metadata

Author(s): Jeyapalan, J., Saretzki, G., Leake, A., Tilby, M.J., Von Zglinicki, T.

Publication type: Article

Publication status: Published

Journal: International Journal of Cancer

Year: 2006

Volume: 118

Issue: 11

Pages: 2727-2734

Print publication date: 01/06/2006

ISSN (print): 0020-7136

ISSN (electronic): 1097-0215


DOI: 10.1002/ijc.21675

PubMed id: 16381006


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