Document Detail


Expression profiling identifies three pathways altered in cellular immortalization: interferon, cell cycle, and cytoskeleton.
MedLine Citation:
PMID:  16960018     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Abrogation of cellular senescence, resulting in immortalization, is a necessary step in the tumorigenic transformation of a cell. Four independent, spontaneously immortalized Li-Fraumeni syndrome (LFS) cell lines were used to analyze the gene expression changes that may have given these cell lines the growth advantage required to become immortal. A cellular senescence-like phenotype can be induced in immortal LFS cells by treating them with the DNA methyltransferase (DNMT) inhibitor 5-aza-deoxycytidine. We hypothesized, therefore, that genes epigenetically silenced by promoter methylation are potentially key regulators of senescence. We used microarrays to compare the epigenetic gene expression profiles of precrisis LFS cells with immortal LFS cells. Gene ontology analysis of the expression data revealed a statistically significant contribution of interferon pathway, cell cycle, and cytoskeletal genes in the process of immortalization. The identification of the genes and pathways regulating immortalization will lead to a better understanding of cellular immortalization and molecular targets in cancer and aging.
Authors:
Aviva Levine Fridman; Lin Tang; Olga I Kulaeva; Bin Ye; Qunfang Li; Fatimah Nahhas; Paul C Roberts; Susan J Land; Judith Abrams; Michael A Tainsky
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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:  The journals of gerontology. Series A, Biological sciences and medical sciences     Volume:  61     ISSN:  1079-5006     ISO Abbreviation:  J. Gerontol. A Biol. Sci. Med. Sci.     Publication Date:  2006 Sep 
Date Detail:
Created Date:  2006-09-08     Completed Date:  2006-10-12     Revised Date:  2013-06-03    
Medline Journal Info:
Nlm Unique ID:  9502837     Medline TA:  J Gerontol A Biol Sci Med Sci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  879-89     Citation Subset:  AIM; IM    
Affiliation:
Program in Molecular Biology and Human Genetics, Barbara Ann Karmanos Cancer Institute, and Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, 110 East Warren Ave., Detroit, Michigan 48201, USA.
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MeSH Terms
Descriptor/Qualifier:
Azacitidine / analogs & derivatives,  pharmacology
Cell Aging
Cell Cycle
Cell Line, Tumor
Cytoskeleton / genetics
DNA Methylation
Down-Regulation
Enzyme Inhibitors / pharmacology
Epigenesis, Genetic*
Female
Fibroblasts / metabolism
Gene Expression Profiling*
Genes, p53
Humans
Interferon Regulatory Factor-7 / metabolism
Interferon-alpha / metabolism
Interferon-beta / metabolism
Li-Fraumeni Syndrome / genetics*,  metabolism
Male
Oligonucleotide Array Sequence Analysis
Reverse Transcriptase Polymerase Chain Reaction
Up-Regulation
Grant Support
ID/Acronym/Agency:
P30CA022453/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Enzyme Inhibitors; 0/Interferon Regulatory Factor-7; 0/Interferon-alpha; 320-67-2/Azacitidine; 77238-31-4/Interferon-beta; 776B62CQ27/decitabine

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


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