Cadherin-11 expression is upregulated in invasive human breast cancer

被引:19
|
作者
Pohlodek, Kamil [1 ]
Tan, Yen Y. [2 ]
Singer, Christian F. [2 ]
Gschwantler-Kaulich, Daphne [2 ]
机构
[1] Comenius Univ, Dept Gynecol & Obstet 2, Fac Med, Ruzinovska 6, Bratislava 82606, Slovakia
[2] Med Univ Vienna, Dept Obstet & Gynecol, Ctr Comprehens Canc, A-1090 Vienna, Austria
关键词
cadherin-11; breast cancer; normal breast tissue; EPITHELIAL-MESENCHYMAL TRANSITION; CATENIN; COHORT; CELLS;
D O I
10.3892/ol.2016.5236
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Loss of expression of cadherin-11 protein is correlated with a loss of epithelial phenotype and a gain in tumor cell proliferation and invasion. It has been hypothesized that cadherin-11 may be a molecular marker for a more aggressive subtype of breast cancer. The present study examined the expression of the mesenchymal gene/protein cadherin-11 in malignant, benign and healthy breast cancer samples. A paraffin-embedded tissue microarray of both malignant and benign/healthy breast tumor was used. Clinicopathological parameters, including age, grading, tumor size, hormone receptors and HER2 receptors status were obtained from patient medical records. Expression of cadherin-11 was analyzed using the monoclonal mouse anti cadherin-11 IgG2B clone. Total RNA was extracted from each breast cancer sample and subjected to semi-quantitative RT-PCR analysis for cadherin-11. Cadherin-11 was detected in 80/82 malignant breast cancer samples and in 33/70 non-malignant tissue samples. Cadherin-11 expression was observed to be predominantly localized to the membrane of tumor cells. When compared to healthy breast tissue biopsies, both cadherin-11 mRNA and protein were demonstrated to be significantly overexpressed in breast carcinoma (P=0.040 and P<0.0001, respectively). Within malignant tumors, however, protein expression was not identified to be associated with other clinicopathological parameters. Our results indicate that cadherin-11 expression is upregulated in malignant human breast cancer.
引用
收藏
页码:4393 / 4398
页数:6
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