Document Detail


Spontaneous tumorigenicity of primary human oral keratinocytes with human papillomavirus negativity and impaired apoptosis.
MedLine Citation:
PMID:  20428774     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Although >60% of oral cancer cases are not related to human papillomavirus (HPV) infection, most studies of oral carcinogenesis in human cells in vitro are carried out with human oral keratinocytes immortalized by HPV DNA. To explore whether human oral keratinocytes can spontaneously transform without HPV infection, we attempted to establish spontaneously immortalized and tumorigenic-transformed human oral keratinocytes by serial subculture to the post-mitotic stage. Here we report two spontaneously transformed human oral keratinocyte lines from adult human gingival samples. These lines were obviously immortal (>140 passages) and transformed phenotypes in vitro. One of the lines, Spi-HOK1, remained non-tumorigenic in nude mice, whereas the other line, Spt-HOK80, showed tumorigenicity. These lines showed epithelial origi-nality, but did not contain high-risk types of HPV DNAs. On karyotyping, Spi-HOK1 was aneuploid with a unique stable marker chromosome. Both cell lines revealed a mutation in the p53 gene, loss of p21WAF1/Cip1 and overexpression of p-Rb-Ser807/811. These cell lines were resistant to cisplatin-induced apoptosis by suppressing induction of apoptotic proteins. These results clearly demonstrate that spontaneous immortalization and spontaneous tumorigenic transformation of primary human oral keratinocytes can occur in vitro without HPV infection and are associated with chromosomal alterations, p53 mutation and impaired apoptosis. To our knowledge, this is the first report demonstrating that the Spi-HOK1 and Spt-HOK80 lines are novel cell lines that are spontaneously transformed from primary human oral keratinocytes.
Authors:
Da Hyun Jang; Ju-Eun Oh; Hyun Ki Kang; O Bok Kim; Seung-Ki Min; Sung Youn Jung; Seong-Doo Hong; Jae-Il Lee; Byung-Moo Min
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  International journal of oncology     Volume:  36     ISSN:  1791-2423     ISO Abbreviation:  Int. J. Oncol.     Publication Date:  2010 Jun 
Date Detail:
Created Date:  2010-04-29     Completed Date:  2010-08-20     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9306042     Medline TA:  Int J Oncol     Country:  Greece    
Other Details:
Languages:  eng     Pagination:  1491-501     Citation Subset:  IM    
Affiliation:
Department of Oral Biochemistry, Seoul National University School of Dentistry, Seoul 110-749, Korea.
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MeSH Terms
Descriptor/Qualifier:
Adult
Animals
Apoptosis / genetics*
Blotting, Western
Cell Line
Cell Separation
Cell Transformation, Neoplastic / genetics*,  pathology
Cyclin-Dependent Kinase Inhibitor p21 / genetics
Flow Cytometry
Gingiva / pathology*
Humans
Immunohistochemistry
Keratinocytes / pathology*
Mice
Mice, Nude
Mouth Mucosa / pathology
Mouth Neoplasms / genetics*,  pathology
Papillomaviridae
Retinoblastoma Protein / genetics
Reverse Transcriptase Polymerase Chain Reaction
Tumor Suppressor Protein p53 / genetics
Xenograft Model Antitumor Assays
Chemical
Reg. No./Substance:
0/CDKN1A protein, human; 0/Cyclin-Dependent Kinase Inhibitor p21; 0/Retinoblastoma Protein; 0/Tumor Suppressor Protein p53

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