Original Paper

Journal of Cancer Research and Clinical Oncology

, Volume 133, Issue 2, pp 83-92

First online:

Dominant-negative E-cadherin inhibits the invasiveness of inflammatory breast cancer cells in vitro

  • Hui-Ming DongAffiliated withDepartment of Breast Surgery, Breast Cancer Institute, Cancer Hospital/Cancer Institute, Fudan University
  • , Gang LiuAffiliated withDepartment of Breast Surgery, Breast Cancer Institute, Cancer Hospital/Cancer Institute, Fudan University
  • , Yi-Feng HouAffiliated withDepartment of Breast Surgery, Breast Cancer Institute, Cancer Hospital/Cancer Institute, Fudan University
  • , Jiong WuAffiliated withDepartment of Breast Surgery, Breast Cancer Institute, Cancer Hospital/Cancer Institute, Fudan University
  • , Jin-Song LuAffiliated withDepartment of Breast Surgery, Breast Cancer Institute, Cancer Hospital/Cancer Institute, Fudan University
  • , Jian-Min LuoAffiliated withDepartment of Breast Surgery, Breast Cancer Institute, Cancer Hospital/Cancer Institute, Fudan University
  • , Zhen-Zhou ShenAffiliated withDepartment of Breast Surgery, Breast Cancer Institute, Cancer Hospital/Cancer Institute, Fudan University
  • , Zhi-Ming ShaoAffiliated withDepartment of Breast Surgery, Breast Cancer Institute, Cancer Hospital/Cancer Institute, Fudan University Email author 

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Abstract

E-cadherin is a transmembrane glycoprotein which mediates epithelial cell-to-cell adhesion function as a tumor suppressor and frequently loss of expression in a wide spectrum of human cancer. However, recent studies demonstrated that E-cadherin was always over-expressed in inflammatory breast cancer (IBC) specimen and cell lines, which is a clinical extreme malignancy of breast cancer. It is hypothesized that the gain and not the loss of the E-cadherin axis contributes to the IBC unique phenotype. To test this assumption, we generated dominant negative mutant E-cadherin high-expression inflammatory breast cancer cells by introduced dominant negative mutant E-cadherin (H-2kd-E-cad) cDNA into human IBC SUM149 cells. Our studies demonstrated that the ability of invasion of SUM149 cells was significantly inhibited by H-2kd-E-cad via down-regulation of MMP-1 and MMP-9 expression. The underlying signal pathway of MAPK phosphorylated Erk 1/2(P44/42) in H-2kd-E-cad-transfected SUM149 cells was significantly down-regulated compared to parental and mock contrast. Our studies provided further functional evidence as the gain of E-cadherin expression dedicated to the IBC malignant phenotype and the blockage of MAPK/Erk activation maybe a promising therapeutic target.

Keywords

E-cadherin Inflammatory breast cancer MMP MAPK