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  • Title: [Correlation among expression of E-cadherin, beta-catenin, and cyclin D1 in breast cancers].
    Author: Yang JF, Chen SL, Liu ZH, Zhang Y.
    Journal: Ai Zheng; 2004 Jul; 23(7):799-802. PubMed ID: 15248915.
    Abstract:
    BACKGROUND & OBJECTIVE: E-cadherin links to the cytoskeleton via catenins and mediates cell-cell homophilic adhesion. beta-catenin not only regulates cell-cell adhesion as a protein interacting with cadherin, but also functions as an important component of the Wnt signaling pathway which has been found to be closely associated with tumor formation. This study was performed to examine the expression of E-cadherin, beta-catenin, and cyclin D1 in breast cancer in order to evaluate their possible roles in the formation and progression of breast cancer. METHODS: The alterations of E-cadherin, beta-catenin, and cyclin D1 in 60 cases of breast cancer were determined using highly sensitive SP immunohistochemical method. RESULTS: Normal immunoreactivity of E-cadherin and beta-catenin were observed in 29 (48.3%) and 18 (30.0%) cases, respectively. Twenty-eight cases (46.7%) showed cyclin D1 overexpression. Thirty percent (9/29) of the cases with normal staining of E-cadherin showed overexpression of cyclin D1, while 61.3%(19/31) of the cases showed overexpression of cyclin D1 with abnormal staining of E-cadherin. Abnormal expression of E-cadherin and overexpression of cyclin D1 showed a significantly positive correlation (rs=0.303,P< 0.05). Forty-two cases showed abnormal staining of beta-catenin. Cyclin D1 overexpression was observed in 57.1% (24/42) of these cases with abnormal staining of beta-catenin, but only observed in 22.2% (4/18) of these cases with normal membranous staining of beta-catenin. There was a significantly positive correlation between the abnormal expression of beta-catenin and overexpression of cyclin D1 (rs=0.321, P< 0.05). CONCLUSION: Down-regulation of E-cadherin and beta-catenin accumulation in the cytoplasm/nuclear may promote malignant transformation and progression by triggering cyclin D1 overexpression in breast cancer.
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