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Potent induction of wild-type p53-dependent transcription in tumour cells by a synthetic inhibitor of cyclin-dependent kinases

Basic information
Original title:Potent induction of wild-type p53-dependent transcription in tumour cells by a synthetic inhibitor of cyclin-dependent kinases
Authors:Vladimír Kotala, S. Uldrijan, Marcel Horký, M. Trbušek, M. Strnad, Bořivoj Vojtěšek
Further information
Citation:KOTALA, Vladimír, S. ULDRIJAN, Marcel HORKÝ, M. TRBUŠEK, M. STRNAD a Bořivoj VOJTĚŠEK. Potent induction of wild-type p53-dependent transcription in tumour cells by a synthetic inhibitor of cyclin-dependent kinases. Cellular and Molecular Life Sciences, Bäsel: Birkhaeuser Verlag, 2001, roč. 58, č. 9, s. 1333-1339. ISSN 1420-682X.Export BibTeX
@article{403490,
author = {Kotala, Vladimír and Uldrijan, S. and Horký, Marcel and Trbušek, M. and Strnad, M. and Vojtěšek, Bořivoj},
article_location = {Bäsel},
article_number = {9},
language = {eng},
issn = {1420-682X},
journal = {Cellular and Molecular Life Sciences},
title = {Potent induction of wild-type p53-dependent transcription in tumour cells by a synthetic inhibitor of cyclin-dependent kinases},
volume = {58},
year = {2001}
}
Original language:English
Field:Genetics and molecular biology
Type:Article in Periodical

Activation of the p53 tumour suppressor protein by distinct forms of stress leads to inhibition of cellular proliferation by inducing cell cycle arrest or apoptosis. The cyclin-dependent kinase inhibitor roscovitine has been shown to induce nuclear accumulaciuon of wild-derived cells.We analyzed the response of different human tumour cell lines to roscovitine treatment with respect to their p53 status. Striking induction of wild-type p53 protein and dramatic enhancement of p53-dependent transcription, coinciding with p21 WAF1 induction, was observed in wildtype, but not mutant, p53-bearing tumour cells after treatment with roccovitine. The transcriptional activity of p53 was substantially higher in roscovitine-treated cells than in cells irradiated with ultravioilet C or ionizing radiation, even though all these agents induced a similar amount of p53 accumulation. These results highlight the therapeutic potential of roscovitine as an anticancer drug, especially in tumours retaining a functional wild-type p53 pathway.

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