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RISS 인기검색어
- 검색키워드
- 저자 : Joseph McQuirer (검색결과 1 건)
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Genetic Instability and the Development of Human Oral Cancer
Park, No-Hee,Joseph McQuirer,Frederick Rutherford,Shin, Ki-Hyuk,Liu, Xuan,Guo, Wentong,Bertolami, Charles N. Korean Academy of Oral Biology and the UCLA Dental 1998 International Journal of Oral Biology Vol.23 No.1
We established an in vitro multistep oral carcinogenesis model by sequential exposure of normal human oral keratinocytes (NHOK) to "high risk" human papillomavirus (HPV) and chemical carcinogens. First, we immortalized primary NHOK by transfecting the cells with either cloned HPV-16 or HPV-18 genome. The immortalized human oral keratinocytes (HOK) were further transformed into tumorigenic cells when they were exposed to chemical carcinogens. However, under the same chemical carcinogen exposure, NHOK did not transform. Although the reason for these differences in normal and HPV-immortalized HOK's response to chemical carcinogens remains unknown, we postulate that it may be due to the differences in the cells' ability to maintain genomic integrity. Genomic integrity is normally maintained by the cell's ability (1) to assess the status of the genome at a given time point, (2) to signal cell cycle progression or arrest, and (3) to repair damaged DNA. Disruptions in any of these pathways may ultimately result in the loss of genomic integrity, a hallmark of neoplastic cells. We demonstrated that, in HPV-immortalized HOK, the E6 and E7 oncoproteins of "high risk" HPV disrupt cellular signals and perturb cell cycle control and DNA repair, particularly when challenged by genotoxic agents. Finally, the effect of "high risk" HPV on the stability of cellular chromosomes was indirectly determined by checking the mutation frequency using a shuttle vector plasmid in NHOK and cells harboring "high risk" HPV genome. We found that infection with "high risk" HPV tremendously enhanced the mutation frequency of the shuttle vector. These data indicate that, in NHOK, genomic integrity is maintained through controlling cell cycle progression and DNA repair when challenged by genotoxic stresses, but "high risk" HPV infection, such as HPV-16 or HPV-18, jeopardizes such cell cycle controlling and DNA repair capacities and causes genetic instability.
RISS
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