The relationship of p63 expression with cell proliferation and apoptosis in DMBA-induced hamster buccal pouch carcinogenesis.
- Author:
Jee Hyun PARK
1
;
Won Deok LEE
;
Chul Gi MIN
;
Jin Han KANG
;
Hoon MYUNG
;
Jong Ho LEE
;
Myung Jin KIM
Author Information
1. Department of Oral and Maxillofacial Surgery, College of Dentistry, Seoul National University, Korea. myungkim@plaza.snu.ac.kr
- Publication Type:Original Article
- Keywords:
p63;
PCNA;
Apoptosis;
Hamster;
DMBA
- MeSH:
9,10-Dimethyl-1,2-benzanthracene;
Animals;
Apoptosis*;
Carcinogenesis*;
Cell Proliferation*;
Cricetinae*;
DNA;
Epithelium;
Genes, p53;
Head;
Humans;
In Situ Nick-End Labeling;
Keratinocytes;
Mouth Neoplasms;
Neck;
Proliferating Cell Nuclear Antigen;
Protein Isoforms;
Sequence Homology;
Transcriptional Activation
- From:Journal of the Korean Association of Oral and Maxillofacial Surgeons
2005;31(3):219-227
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: Abnormalities in the p53 gene are regarded as the most consistent genetic abnormalities detected in head and neck squamous cell carcinogenesis. Two new members of the p53 gene family, p73 and p63 have recently been identified. They share considerable sequence homology with p53 in the transactivation, DNA binding, and oligomerization domains, indicating possible involvement in carcinogenesis. Disruption of the homeostatic balance between proliferation and apoptosis is widely believed to contribute to human oral carcinogenesis. The aim of this study was to analyze expression of p63 in squamous cell carcinogenesis and to compare with immunochemical markers representing cell proliferation and apoptosis. MATERIALS AND METHODS: Using the Syrian hamster oral cancer model, the fraction of apoptotic (apoptotic index-AI), proliferating (mitotic index-MI) and p63 expressing keratinocytes were examined at normal, dysplastic and malignant oral epithelium using the TUNEL assay, PCNA and p63 immunostaining. RESULTS: p63 significantly increased between normal and dysplastic epithelium and between dysplastic and malignant epithelium. PCNA significantly increased between normal and dysplastic epithelium and between normal and malignant epithelium. However, increase between dysplastic and malignant epithelium, though still increasing, was not statistically significant. The percentage of TUNEL positive cells increased from normal to dysplastic epithelium and returned to normal keratinocyte level in the malignant epithelium. However, differences between tissue types were not significant. The ratio of MI:AI increased significantly only in the dysplastic-malignant epithelial transition. The increase of p63 expression closely reflected the change in the MI:AI ratio during oral carcinogenesis. CONCLUSION: The p63 may be associated with the regulation of epithelial proliferation and apoptosis in DMBA-induced hamster buccal pouch squamous cell carcinogenesis. Further study is required to investigate which p63 isoforms are involved in hamster buccal pouch carcinogenesis.
