The expression of metalloproteinases is a poor prognostic marker in both BCCs and SCCs, but some PMDs express also MMPs. Matrix metalloproteinases (MMPs) are a family of more than 28 enzymes that were initially identified on the basis of their ability to cleave most elements of the extracellular matrix (ECM), but have subsequently been found to be upregulated in EMT and nearly every tumor type. These results suggest that aberrant p16, RAR-β2, TIMP3, ERCC1, and BRCA1 expression might occur that is inconsistent with the respective gene promoter methylation status, and that this overexpression might serve to promote the inflammatory carcinogenesis caused by C. ERCC1 and BRCA1 promoters were not methylated at any stage however, their protein expression disappeared beginning at hyperplasia and nuclear protein re-expression in SCC was observed only for ERCC1. In comparison, TIMP3 protein expression was suppressed during carcino-genesis and RAR-β2 expression was attenuated in the cytoplasm but enhanced in nuclei. TIMP3 and RAR-β2 promoter methyla-tion progressed until the precancerous stage but disappeared upon malignant transformation. We observed nuclear p16 overexpression despite increases in p16 gene promoter methylation during the carcinogenic process. Promoter methylation and protein expression were analyzed by methylation specific PCR and immu-nohistochemical staining, respectively, of 5 areas in the forestomachs of alloxan-induced diabetic rats with hyperplastic candidiasis: normal squamous epithelia, squamous hyperpla-sia, squamous hyperplasia adjacent to SCC, squamous hyperplasia transitioning to SCC, and SCC. In the present study, we investigate whether impaired DNA methylation and associated protein expression of tumor suppressor and DNA repair genes are involved in the SCC carcinogenesis process using this hyperplastic candidiasis model. We have previously produced an animal model for hyperplastic candidiasis in the rat forestomach. albicans is a critical factor in tumor development however, the oncogenic mechanism is unclear. Hyperplastic candidiasis is characterized by thickening of the mucosal epithelia with Can-dida albicans infection with occasional progression to squamous cell carcinoma (SCC).
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