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Tumour-cell apoptosis after cisplat in treatment is not telomere dependent

✍ Scribed by Jessie C. Jeyapalan; Gabriele Saretzki; Alan Leake; Michael J. Tilby; Thomas von Zglinicki

Publisher
John Wiley and Sons
Year
2006
Tongue
French
Weight
934 KB
Volume
118
Category
Article
ISSN
0020-7136

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✦ Synopsis

Abstract

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 inducer of the signal pathway towards apoptosis and/or growth arrest in cisplatin‐treated tumour cells. © 2005 Wiley‐Liss, Inc.

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