Document Detail


Fibroblasts from Werner syndrome patients: cancer cells derived by experimental introduction of oncogenes maintain malignant properties despite entering crisis.
MedLine Citation:
PMID:  20043098     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Werner syndrome (WS) results from defects in the gene encoding WRN RecQ helicase. WS fibroblasts undergo premature senescence in culture. Because cellular senescence is a tumor suppressor mechanism, we examined whether WS fibroblasts exhibited reduced tumorigenicity, in comparison to control cells, in a model of experimental conversion of normal human cells to cancer cells. The combination of oncogenic Ras (Ha-Ras(V12G)) and SV40 large T antigen (SV40 LT) causes human cells to acquire neoplastic properties in the absence of telomerase. We found that WS cells could also be converted to a tumorigenic state by these oncogenes, as evidenced by invasion and metastasis of cells implanted in immunodeficient mice. Ras/SV40 LT-expressing cells retained invasiveness and malignant properties even when cells reached crisis in tumors in vivo. High levels of gelatinase were found by an in situ assay in Ras/SV40 LT-expressing cells undergoing crisis. We conclude that, despite evidence of accelerated senescence in WS cells, there is no evidence that the absence of active WRN acts as a barrier to neoplastic transformation. Moreover, we find that tumorigenic human cells retain malignant properties of the cells as they approach and reach crisis.
Authors:
Furong Yuan; Meizhen Chen; Peter J Hornsby
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Oncology reports     Volume:  23     ISSN:  1791-2431     ISO Abbreviation:  Oncol. Rep.     Publication Date:  2010 Feb 
Date Detail:
Created Date:  2009-12-31     Completed Date:  2010-03-30     Revised Date:  2011-09-22    
Medline Journal Info:
Nlm Unique ID:  9422756     Medline TA:  Oncol Rep     Country:  Greece    
Other Details:
Languages:  eng     Pagination:  377-86     Citation Subset:  IM    
Affiliation:
Department of Physiology, University of Texas Health Science Center, San Antonio, TX 78245, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antigens, Polyomavirus Transforming / genetics,  physiology
Cell Transformation, Neoplastic / genetics,  pathology*
Cells, Cultured
DNA-Binding Proteins / genetics
Disease Progression
Female
Fibroblasts / pathology*
Genes, ras / physiology
Graft Survival
Humans
Immunoglobulin gamma-Chains / genetics
Male
Mice
Mice, Knockout
Neoplasm Transplantation
Neoplasms, Experimental / genetics,  pathology*
Oncogenes / physiology
Transplantation, Heterologous
Werner Syndrome / pathology*
Grant Support
ID/Acronym/Agency:
AG12287/AG/NIA NIH HHS; AG20752/AG/NIA NIH HHS; P01 AG020752-020006/AG/NIA NIH HHS; P30 CA54174/CA/NCI NIH HHS; R37 AG012287-14/AG/NIA NIH HHS
Chemical
Reg. No./Substance:
0/Antigens, Polyomavirus Transforming; 0/DNA-Binding Proteins; 0/Immunoglobulin gamma-Chains; 0/Rag2 protein, mouse

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