Document Detail

Evidence of increased Id-1 expression and its role in cell proliferation in nasopharyngeal carcinoma cells.
MedLine Citation:
PMID:  12203366     Owner:  NLM     Status:  MEDLINE    
Inhibitor of differentiation or DNA binding (Id-1), a helix-loop-helix transcription factor, has recently been shown to inactivate the retinoblastoma (RB)/p16(INK4a) pathway through down-regulation of p16(INK4a) and increasing phosphorylation of RB in certain cell types. Nasopharyngeal carcinoma (NPC) is a common cancer in Hong Kong, and inactivation of the tumor suppressor RB at transcription level is a rare event in NPC. The objective of this study was to investigate the role of Id-1 in NPC cell proliferation and its expression in NPC samples. An NPC cell line, CNE1, was transfected with a retroviral vector containing a full-length Id-1 cDNA, and six stable transfectant clones were isolated with differential Id-1 expression levels. The effect of ectopic Id-1 expression on serum-independent cell growth, cell-cycle distribution, and expression of proteins associated with RB pathway was studied. The Id-1 expression in five NPC samples was also investigated using immunohistochemistry. Ectopic Id-1 expression in CNE1 cells resulted in an increase in serum-independent cell growth, percentage of cells in S phase, and phosphorylation of RB and cyclin-dependent kinase 2 proteins. In addition, immunohistochemical studies on NPC samples showed that expression of Id-1 was present in NPC cells but absent in normal tissues. This study demonstrates that Id-1 plays an important role in cell proliferation in NPC cells, and our results provide evidence for the first time of the significance of Id-1 expression in NPC cells and suggest a possible role of Id-1 expression in the inactivation of RB and development of NPC.
Xianghong Wang; Kexin Xu; Ming Tat Ling; Y C Wong; Hui Chen Feng; John Nicholls; S W Tsao
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Molecular carcinogenesis     Volume:  35     ISSN:  0899-1987     ISO Abbreviation:  Mol. Carcinog.     Publication Date:  2002 Sep 
Date Detail:
Created Date:  2002-08-30     Completed Date:  2002-10-03     Revised Date:  2012-06-25    
Medline Journal Info:
Nlm Unique ID:  8811105     Medline TA:  Mol Carcinog     Country:  United States    
Other Details:
Languages:  eng     Pagination:  42-9     Citation Subset:  IM    
Copyright Information:
Copyright 2002 Wiley-Liss, Inc.
Department of Anatomy, Faculty of Medicine, University of Hong Kong, Hong Kong, SAR, China.
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MeSH Terms
CDC2-CDC28 Kinases*
Carcinoma / metabolism*,  pathology*
Carrier Proteins / metabolism
Cell Cycle
Cell Division
Culture Media, Serum-Free
Cyclin-Dependent Kinase 2
Cyclin-Dependent Kinase 4
Cyclin-Dependent Kinase Inhibitor p27
Cyclin-Dependent Kinases / metabolism
DNA-Binding Proteins / genetics,  metabolism*
Inhibitor of Differentiation Protein 1
Intracellular Signaling Peptides and Proteins*
Nasopharyngeal Neoplasms / metabolism*,  pathology*
Protein-Serine-Threonine Kinases / metabolism
Proto-Oncogene Proteins*
Reference Values
Repressor Proteins*
Retinoblastoma Protein
Transcription Factors / genetics,  metabolism*
Tumor Cells, Cultured
Reg. No./Substance:
0/CDKN1B protein, human; 0/Carrier Proteins; 0/Culture Media, Serum-Free; 0/DNA-Binding Proteins; 0/ID1 protein, human; 0/Inhibitor of Differentiation Protein 1; 0/Intracellular Signaling Peptides and Proteins; 0/Proto-Oncogene Proteins; 0/Repressor Proteins; 0/Retinoblastoma Protein; 0/Transcription Factors; 147604-94-2/Cyclin-Dependent Kinase Inhibitor p27; EC Kinases; EC Kinases; EC protein, human; EC protein, human; EC Kinase 2; EC Kinase 4; EC Kinases

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

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