Microtubule-active drugs taxol, vinblastine, and nocodazole increase the levels of transcriptionally active p53

A range of DNA-damaging agents has been shown to increase cellular levels of the nuclear phosphoprotein p53 and to induce p53-dependent processes. We examined the ability of three microtubule-active agents, taxol, vinblastine, and nocodazole, to increase p53 levels and activate p53-dependent process...

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Bibliographic Details
Published in:Cancer research (Chicago, Ill.) Ill.), 1995-12, Vol.55 (24), p.6021-6025
Main Authors: TISHLER, R. B, LAMPPU, D. M, PARK, S, PRICE, B. D
Format: Article
Language:English
Subjects:
3T3 Cells
Animals
Antineoplastic agents
Base Sequence
Biological and medical sciences
Cell Cycle - drug effects
Cyclin-Dependent Kinase Inhibitor p21
Cyclins - genetics
DNA-Binding Proteins - metabolism
Gene Expression Regulation - drug effects
General aspects
Medical sciences
Mice
Microtubules - drug effects
Molecular Sequence Data
Nocodazole - pharmacology
Oligodeoxyribonucleotides - chemistry
Paclitaxel - pharmacology
Pharmacology. Drug treatments
Promoter Regions, Genetic
RNA, Messenger - genetics
Transcription, Genetic - drug effects
Tumor Suppressor Protein p53 - genetics
Vinblastine - pharmacology
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Summary:A range of DNA-damaging agents has been shown to increase cellular levels of the nuclear phosphoprotein p53 and to induce p53-dependent processes. We examined the ability of three microtubule-active agents, taxol, vinblastine, and nocodazole, to increase p53 levels and activate p53-dependent processes. When tested using a p53 DNA-binding assay, all three agents induced p53 in a dose-dependent manner. To varying degrees, these agents also induced p21WAF1/CIP1 mRNA and transcription in a chloramphenicol acetyl transferase reporter system. These data suggest there is an additional pathway for activating p53 and subsequent p53-dependent processes.
ISSN:0008-5472
1538-7445