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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
9
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pubmed:dateCreated |
2001-10-1
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pubmed:abstractText |
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 accumulation of wild-type p53 in human untransformed and tumour-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 p21WAF1 induction, was observed in wildtype, but not mutant, p53-bearing tumour cells after treatment with roscovitine. The transcriptional activity of p53 was substantially higher in roscovitine-treated cells than in cells irradiated with ultraviolet 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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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antineoplastic Agents,
http://linkedlifedata.com/resource/pubmed/chemical/CDKN1A protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Cdkn1a protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclin-Dependent Kinase Inhibitor...,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclin-Dependent Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclins,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Purines,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Suppressor Protein p53,
http://linkedlifedata.com/resource/pubmed/chemical/roscovitine
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1420-682X
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
58
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1333-9
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:11577989-Animals,
pubmed-meshheading:11577989-Antineoplastic Agents,
pubmed-meshheading:11577989-Breast Neoplasms,
pubmed-meshheading:11577989-Cell Line,
pubmed-meshheading:11577989-Cyclin-Dependent Kinase Inhibitor p21,
pubmed-meshheading:11577989-Cyclin-Dependent Kinases,
pubmed-meshheading:11577989-Cyclins,
pubmed-meshheading:11577989-Enzyme Inhibitors,
pubmed-meshheading:11577989-Female,
pubmed-meshheading:11577989-Fibroblasts,
pubmed-meshheading:11577989-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:11577989-Humans,
pubmed-meshheading:11577989-Kinetics,
pubmed-meshheading:11577989-Melanoma,
pubmed-meshheading:11577989-Mice,
pubmed-meshheading:11577989-Osteosarcoma,
pubmed-meshheading:11577989-Purines,
pubmed-meshheading:11577989-Recombinant Proteins,
pubmed-meshheading:11577989-Transcription, Genetic,
pubmed-meshheading:11577989-Transfection,
pubmed-meshheading:11577989-Tumor Cells, Cultured,
pubmed-meshheading:11577989-Tumor Suppressor Protein p53
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pubmed:year |
2001
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pubmed:articleTitle |
Potent induction of wild-type p53-dependent transcription in tumour cells by a synthetic inhibitor of cyclin-dependent kinases.
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pubmed:affiliation |
Department of Experimental Oncology, Masaryk Memorial Cancer Institute, Brno, Czech Republic.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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