Document Detail


Association of p16(INK4a) and pRb inactivation with immortalization of human cells.
MedLine Citation:
PMID:  12507935     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
To examine the association of cell cycle regulatory gene inactivation with human cell immortalization, we determined the expression status of INK4a, Rb, and WAF1/ CIP1, in eleven in vitro immortalized human cell lines, including fibroblasts and keratinocytes. Two human papillomavirus type 16 E6 expressing cell lines with telomerase activity, including a fibroblast cell line and a keratinocyte cell line, expressed no detectable p16(INK4a). These cell lines had a hyperphosphorylated pRb and reduced expression of p21(WAF1/CIP1). All of seven fibroblast cell lines immortalized either spontaneously or by (60)Co, X-rays, 4-nitroquinoline 1-oxide or aflatoxin B(1), maintaining their telomeres by the ALT (alternative lengthening of telomeres) pathway, displayed loss of expression of p16(INK4a) and hyperphosphorylation of pRb. Levels of p21(WAF1/CIP1) expression varied among the cell lines. Two fibroblast cell lines that became immortalized following infection with a retrovirus vector encoding human telomerase catalytic subunit (hTERT) cDNA were also accompanied by inactivation of p16(INK4a) and pRb pathways. Acquisition of telomerase activity alone was not sufficient for immortalization of these cell lines. Taken together, all the cell lines including fibroblasts and keratinocytes, with either telomerase activity or the ALT pathway for telomere maintenance showed loss of expression of p16(INK4a) and hyperphosphorylation of pRb. These demonstrate the association of inactivation of both p16(INK4a) and pRb with immortalization of human cells including fibroblasts and epithelial cells and telomerase-positive cells and ALT-positive cells.
Authors:
Takeki Tsutsui; Shin-Ichi Kumakura; Akito Yamamoto; Hideaki Kanai; Yukiko Tamura; Takashi Kato; Masanori Anpo; Hidetoshi Tahara; J Carl Barrett
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Carcinogenesis     Volume:  23     ISSN:  0143-3334     ISO Abbreviation:  Carcinogenesis     Publication Date:  2002 Dec 
Date Detail:
Created Date:  2002-12-31     Completed Date:  2003-02-10     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8008055     Medline TA:  Carcinogenesis     Country:  England    
Other Details:
Languages:  eng     Pagination:  2111-7     Citation Subset:  IM    
Affiliation:
Department of Pharmacology, The Nippon Dental University, School of Dentistry at Tokyo, Japan.
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MeSH Terms
Descriptor/Qualifier:
4-Nitroquinoline-1-oxide
Aflatoxin B1
Carcinogens
Cell Cycle
Cell Line
Cell Transformation, Neoplastic
Cobalt Radioisotopes
Cyclin-Dependent Kinase Inhibitor p16 / metabolism*
Cyclin-Dependent Kinase Inhibitor p21
Cyclins / metabolism
DNA, Complementary / metabolism
DNA-Binding Proteins
Fibroblasts / metabolism
Humans
Keratinocytes / metabolism
Oncogene Proteins, Viral / metabolism
Phosphorylation
RNA, Messenger / metabolism
Repressor Proteins*
Retinoblastoma Protein / metabolism*
Reverse Transcriptase Polymerase Chain Reaction
Telomerase / metabolism
Telomere
Time Factors
Tumor Cells, Cultured
X-Rays
Chemical
Reg. No./Substance:
0/CDKN1A protein, human; 0/Carcinogens; 0/Cobalt Radioisotopes; 0/Cyclin-Dependent Kinase Inhibitor p16; 0/Cyclin-Dependent Kinase Inhibitor p21; 0/Cyclins; 0/DNA, Complementary; 0/DNA-Binding Proteins; 0/E6 protein, Human papillomavirus type 16; 0/Oncogene Proteins, Viral; 0/RNA, Messenger; 0/Repressor Proteins; 0/Retinoblastoma Protein; 1162-65-8/Aflatoxin B1; 56-57-5/4-Nitroquinoline-1-oxide; EC 2.7.7.49/Telomerase

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


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