| Telomeric plasmid induces human cancer cell dysfunction depending on ATM activity. | |
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MedLine Citation:
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PMID: 20535839 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Telomeres are essential for chromosome stability and the regulation of the replicative life-span of somatic cells. Many studies showed that exogenous telomeric repeats could activate p53 protein. It is not known how cell dysfunction is induced by telomeric plasmids. A covalent closed circular (ccc) double-stranded plasmid containing (TTAGGG)(96) repeats (pRST5) was transiently transfected into the human gastric cancer MGC-803 cells. We first confirmed that the cell viabilities decreased by 27%, cell senescence increased by 62% and G2/M cycle arrested in pRST5 plasmid transfected cells. Compared to control groups, cells transfected with telomeric plasmids showed an ATM-dependent increasing of p53, TRF1, and TRF2 expression. Furthermore, telomere dysfunction-induced foci (TIF) were observed. In conclusion, telomeric plasmids can elicit endogenous telomere dysfunction and induce cell senescence by activating ATM-p53 pathway. |
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Authors:
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Xiao-Fei Guo; En-Hua Cao |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Cell biochemistry and function Volume: 28 ISSN: 1099-0844 ISO Abbreviation: Cell Biochem. Funct. Publication Date: 2010 Jul |
Date Detail:
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Created Date: 2010-07-05 Completed Date: 2010-10-20 Revised Date: 2011-11-02 |
Medline Journal Info:
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Nlm Unique ID: 8305874 Medline TA: Cell Biochem Funct Country: England |
Other Details:
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Languages: eng Pagination: 381-6 Citation Subset: IM |
Copyright Information:
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Copyright 2010 John Wiley & Sons, Ltd. |
Affiliation:
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Institute of Biophysics, Chinese Academy of Sciences, Graduate School of the Chinese Academy of Sciences, Chaoyang District, Beijing, PR China. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Cell Aging* Cell Cycle Proteins / metabolism* Cell Division Cell Line, Tumor DNA-Binding Proteins / metabolism* G2 Phase Humans Plasmids / genetics* Protein-Serine-Threonine Kinases / metabolism* RNA Interference RNA, Small Interfering Stomach Neoplasms / metabolism Telomere / chemistry*, metabolism Telomeric Repeat Binding Protein 1 / metabolism Telomeric Repeat Binding Protein 2 / metabolism Transfection Tumor Suppressor Protein p53 / metabolism Tumor Suppressor Proteins / metabolism* |
| Chemical | |
Reg. No./Substance:
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0/Cell Cycle Proteins; 0/DNA-Binding Proteins; 0/RNA, Small Interfering; 0/Telomeric Repeat Binding Protein 1; 0/Telomeric Repeat Binding Protein 2; 0/Tumor Suppressor Protein p53; 0/Tumor Suppressor Proteins; EC 2.7.11.1/Protein-Serine-Threonine Kinases; EC 2.7.11.1/ataxia telangiectasia mutated protein |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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