NDLI: Temozolomide induces senescence but not apoptosis in human melanoma cells

Content Provider	PubMed Central
Author	Mhaidat, N. M. Allen, J. Avery-kiejda, K. A. Scott, R. J. Hersey, P. Zhang, X. D.
Copyright Year	2007
Abstract	Temozolomide (TMZ), a DNA alkylating agent used in the treatment of melanoma, is believed to mediate its effect by addition of a methyl group to the O6 position of guanine in DNA. Resistance to the agent may be in part due to the activity of O6-methylguanine-DNA methyl transferase (MGMT). In the present study, we show that sensitivity of melanoma cells to TMZ was dependent on their p53 status and levels of MGMT. Analysis of the mechanisms underlying reduced viability showed no evidence for induction of apoptosis even though marked levels of apoptosis was seen in TK6 lymphoma cells. Sensitivity of melanoma cells was associated with p53-dependent G2/M cell cycle arrest and induction of senescence. To verify the role of p53, the assays were repeated in presence of pifithrin-α, an inhibitor of p53. This resulted in increased viability of melanoma cells with wild-type p53 and reversed G2/M cell cycle arrest. Paradoxically, apoptosis was increased in melanoma but decreased as expected in TK6 lymphoma cells. These results are consistent with the view that TMZ is relatively ineffective against melanoma due to defective apoptotic signalling resulting from activation of p53. The nature of the defects in apoptotic signalling remains to be explored.
Related Links	http://dx.doi.org/10.1038/sj.bjc.6604017
Ending Page	1233
Page Count	9
Starting Page	1225
File Format	PDF
ISSN	00070920
e-ISSN	15321827
Journal	British Journal of Cancer
Issue Number	9
Volume Number	97
Language	English
Publisher	Nature Publishing Group
Publisher Date	2007-11-05
Access Restriction	Open
Rights Holder	Nature Publishing Group
Subject Keyword	Cancer Research Oncology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cancer Research Oncology

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