Abstract
Background: Epidermal growth factor receptor (EGFR) and c-Jun oncogenes are implicated in the same pathway of signal transduction affecting cell differentiation. In order to investigate their possible correlation with sequential histological stages of OSCC formation, we established an experimental model of induced oral carcinogenesis in Syrian golden hamsters. Materials and Methods: Thirty-seven animals were divided into one control group (n=7) and three experimental groups (n=10 each), which were treated with a carcinogen and sacrificed at 10, 14 and 19 weeks after treatment. Tumour sections were studied using monoclonal antibodies against EGFR and c-Jun proteins. Results: The same pattern of expression was observed for both oncogenes, with a significant gradual increase of positively stained cells throughout oral carcinogenesis. Conclusion: Since EGFR and c-Jun are implicated in the same molecular pathway of signal transduction, it may be assumed that an increase in EGFR levels leads to increased activation of phospholipase Cγ signal transduction cascade, which in turn activates c-Jun protein. Therefore, c-Jun expression in oral cancer seems to be increased through the EGFR-PLCγ-Raf-MEK-ERK pathway and not the H-ras-Raf-MEK-ERK/JNK pathway.
Footnotes
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↵* Both authors contributed equally to this work.
- Received June 14, 2007.
- Revision received July 19, 2007.
- Accepted July 25, 2007.
- Copyright © 2007 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved