Publication details
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 and Bořivoj VOJTĚŠEK. Potent induction of wild -type
p53 -dependent transcription in tumour cells by a synthetic
inhibitor of cyclin -dependent kinases (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, vol.
58, No 9, p. 1333 -1339. ISSN 1420 -682X.Export BibTeX |
| 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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