Purpose: The aim of this study was to cast light on initiating molecular events associated with the developmentof premalignant oral lesions induced by tobacco and/or areca nut.
Method: Immunohistochemical analyses ofcell cycle regulatory proteins (LIMD1, RBSP3, p16, RB, phosphorylated RB, p53), EGFR and SH3GL2 (EGFRassociated protein) were performed with inflammatory/ ulcerative epithelium and adjacent hyperplastic/milddysplastic lesions.
Results: No change in expression of the proteins was seen in inflammatory epithelium. Reducednuclear expression of LIMD1 was evident in ulcerative epithelium. In hyperplastic lesions, reduced expression ofRBSP3, p16, SH3GL2 and overexpression of p-RB and EGFR were apparent. Reduced nuclear expression of p53was observed in mild dysplastic lesions.
Conclusion: Our data suggest that inactivation of LIMD1 in ulcerativeepithelium might predispose the tissues to alterations of other cell cycle regulatory and EGFR signaling proteinsneeded for the development of premalignant oral lesions.