Concomitant loss of p120-catenin and ?-catenin membrane expression and oral carcinoma progression with E-cadherin reduction.

ABSTRACT: The binding of p120-catenin and ?-catenin to the cytoplasmic domain of E-cadherin establishes epithelial cell-cell adhesion. Reduction and loss of catenin expression degrades E-cadherin-mediated carcinoma cell-cell adhesion and causes carcinomas to progress into aggressive states. Since both catenins are differentially regulated and play distinct roles when they dissociate from E-cadherin, evaluation of their expression, subcellular localization and the correlation with E-cadherin expression are important subjects. However, the same analyses are not readily performed on squamous cell carcinomas in which E-cadherin expression determines the disease progression. In the present study, we examined expression and subcellular localization of p120-catenin and ?-catenin in oral carcinomas (n = 67) and its implications in the carcinoma progression and E-cadherin expression using immunohitochemistry. At the invasive front, catenin-membrane-positive carcinoma cells were decreased in the dedifferentiated (p120-catenin, P < 0.05; ?-catenin, P < 0.05) and invasive carcinomas (p120-catenin, P < 0.01; ?-catenin, P < 0.05) and with the E-cadherin staining (p120-catenin, P < 0.01; ?-catenin, P < 0.01). Carcinoma cells with ?-catenin cytoplasmic and/or nuclear staining were increased at the invasive front compared to the center of tumors (P < 0.01). Although the p120-catenin isoform shift from three to one associates with carcinoma progression, it was not observed after TGF-?, EGF or TNF-? treatments. The total amount of p120-catenin expression was decreased upon co-treatment of TGF-? with EGF or TNF-?. The above data indicate that catenin membrane staining is a primary determinant for E-cadherin-mediated cell-cell adhesion and progression of oral carcinomas. Furthermore, it suggests that loss of p120-catenin expression and cytoplasmic localization of ?-catenin fine-tune the carcinoma progression.

SUBMITTER: Sasaya K 

PROVIDER: S-EPMC3735538 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature