EGFR and c-Jun exhibit the same pattern of expression and increase gradually during the progress of oral oncogenesis

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.

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.

The same pattern of expression was observed for both oncogenes, with a significant gradual increase of positively stained cells throughout oral carcinogenesis.

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 Cy signal transduction cascade, which in turn activates c-Jun protein. Therefore, c-Jun expression in oral cancer seems to be increased through the EGFR-PLCy-Raf-MEK-ERK pathway and not the H-ras-Raf-MEK-ERK/JNK pathway.