Abstract

Introduction: E-cadherin is an intercellular adhesion molecule, whose loss of expression may facilitate the process of cancer invasion and metastasis. Although the expression of E-cadherin has been widely studied in primary breast cancers, little is known about its expression at the corresponding metastatic lymph node. Here we comparatively studied their E-cadherin expression patterns and related them to the pathological data of breast cancer patients. Methods: Only lymph nodes which were pathologically identified as metastases were included in this study to pair up the primary tumors. The quantitative real-time PCR (Q-RT-PCR) technique was used to assess the Ecadherin RNA expression levels in invasive ductal breast cancer subjects. E-cadherin gene copies were normalized using beta-actin gene copies. ER, PR, cerbB2 expressions in the primary tumor were routinely examined by immunohistochemistry method. Tumor characteristics and number of metastatic lymph nodes were gathered from the pathology reports. Results: We tried to explore the relationship between E-cadherin expression in 21 primary tumors and their corresponding metastatic lymph nodes. However, the Q-RT-PCR data shows that an aberrant expression exists in both primary tumors and the corresponding lymph nodes (p=0.115), in which metastatic lymph nodes showed slight higher gene copies comparing to primary sites (77.77 ± 94.74vs43.35 ± 40.03, respectively). It is noteworthy that nodal E-cadherin expression was closely but negatively correlated with tumor size (p 0.05). Conclusions: These study shows that E-cadherin expression is aberrant in invasive ductal cancers and their corresponding metastatic lymph nodes. E-cadherin expression in the metastasized lymph node is closely related to tumor size and number of metastasized lymph nodes.

Highlights

  • E-cadherin is an intercellular adhesion molecule, whose loss of expression may facilitate the process of cancer invasion and metastasis

  • An aberrant expression exists in both primary tumors and the corresponding lymph nodes, in which metastatic lymph nodes showed slight higher gene copies comparing to primary sites (77.77 ± 94.74 vs 43.35 ± 40.03, respectively)

  • It is noteworthy that nodal E-cadherin expression was closely but negatively correlated with tumor size (p

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Summary

Introduction

E-cadherin is an intercellular adhesion molecule, whose loss of expression may facilitate the process of cancer invasion and metastasis. We comparatively studied their E-cadherin expression patterns and related them to the pathological data of breast cancer patients. Tumor invasion with subsequent metastases is one of major cause of morbidity and mortality in patients with breast cancer. Detachment of cell-cell adhesion is indispensable for the first step of invasion and metastasis of cancer. This mechanism is frequently associated with the impairment of either E-cadherin expression or function [2]. E-cadherin is one of calcium-dependent transmembrane glycoprotein mediating cell-cell adhesion, involved in epithelial cell-to-cell adhesion [3]. The E-cadherin gene, located on chromosome 16q22.1, is an important regulator of morphogenesis [4,5,6]

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