Document Detail

Heat shock factor 1-mediated aneuploidy requires a defective function of p53.
MedLine Citation:
PMID:  19934326     Owner:  NLM     Status:  MEDLINE    
Because heat shock factor 1 (HSF1) phosphorylation by Plk1 has been previously reported to be involved in mitotic regulation and p53 function may be involved in this mitotic regulation, we have further examined HSF1 functions in mitotic regulation according to p53 status. Nocodazole-mediated aneuploidy was increased in p53-defective (p53Mut) cells; however, it was not increased in p53 wild-type (p53WT) cells. Phosphorylation of HSF1 at Ser216 was increased in p53Mut cells with increased stability of securin and cyclin B1 in mitosis compared with p53WT cells. The interaction of p53 with Plk1 that was shown in p53WT cells and that induced normal mitotic checkpoint function was not observed in p53Mut cells; instead, the binding of HSF1 with Plk1 and HSF1 phosphorylation at Ser216 were seen in p53Mut cells, which resulted in increased aneuploidy production. Moreover, the interaction affinity of Cdc20 with Mad2 was inhibited in p53Mut cells, whereas the interaction between Cdc20 and HSF1 was increased. From the data, it was suggested that HSF1-mediated aneuploidy was more facilitated in p53-defective cells, indicating the importance of novel mechanisms for p53 function in HSF1-mediated mitotic regulation and genomic instability.
Eun-Ho Kim; Yoon-Jin Lee; Sangwoo Bae; Jae Seon Lee; Joon Kim; Yun-Sil Lee
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Cancer research     Volume:  69     ISSN:  1538-7445     ISO Abbreviation:  Cancer Res.     Publication Date:  2009 Dec 
Date Detail:
Created Date:  2009-12-16     Completed Date:  2010-01-05     Revised Date:  2011-11-02    
Medline Journal Info:
Nlm Unique ID:  2984705R     Medline TA:  Cancer Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  9404-12     Citation Subset:  IM    
Division of Radiation Effects, Korea Institute of Radiological and Medical Sciences, Seoul, Korea.
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MeSH Terms
Bone Neoplasms / drug therapy,  genetics,  metabolism
Calcium-Binding Proteins / metabolism
Carcinoma, Non-Small-Cell Lung / drug therapy,  genetics,  metabolism
Cell Cycle Proteins / antagonists & inhibitors,  metabolism
Cell Line, Tumor
DNA-Binding Proteins / antagonists & inhibitors,  genetics*,  metabolism*
HCT116 Cells
Lung Neoplasms / drug therapy,  genetics,  metabolism
Mice, Knockout
Nocodazole / pharmacology
Osteosarcoma / drug therapy,  genetics,  metabolism
Protein Binding
Protein-Serine-Threonine Kinases / antagonists & inhibitors,  metabolism
Proto-Oncogene Proteins / antagonists & inhibitors,  metabolism
Repressor Proteins / metabolism
Transcription Factors / antagonists & inhibitors,  genetics*,  metabolism*
Tumor Suppressor Protein p53 / genetics,  metabolism*
Reg. No./Substance:
0/Calcium-Binding Proteins; 0/Cell Cycle Proteins; 0/DNA-Binding Proteins; 0/MAD2L1 protein, human; 0/Proto-Oncogene Proteins; 0/Repressor Proteins; 0/TP53 protein, human; 0/Transcription Factors; 0/Tumor Suppressor Protein p53; 0/heat shock transcription factor; 156288-95-8/CDC20 protein, human; 31430-18-9/Nocodazole; EC Kinases; EC kinase 1

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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