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$CDH_3$/P-Cadherin regulates migration of $HuCCT_1$ cholangiocarcinoma cells

  • Baek, Sung-Min (Department of Anatomy, School of Medicine, Pusan National University) ;
  • Lee, Yong-Whan (Department of Anatomy, School of Medicine, Pusan National University) ;
  • Yoon, Sik (Department of Anatomy, School of Medicine, Pusan National University) ;
  • Baek, Sun-Yong (Department of Anatomy, School of Medicine, Pusan National University) ;
  • Kim, Bong-Seon (Department of Anatomy, School of Medicine, Pusan National University) ;
  • Oh, Sae-Ock (Department of Anatomy, School of Medicine, Pusan National University)
  • Received : 2010.04.04
  • Accepted : 2010.05.12
  • Published : 2010.06.30

Abstract

Intrahepatic cholangiocarcinoma is the second most common subtype of primary hepatobilliary cancer. Despite advances in surgical and medical therapy, its survival rate remains poor. Compared to hepatocellular carcinoma (HCC), the most common liver malignancy, the underlying mechanisms of cholangiocarcinoma carcinogenesis are poorly characterized. P-cadherin (CDH3) is a cadherin super family member. Although CDH3 is frequently over-expressed in cholangiocarcinoma tissues, its roles have never been characterized. To determine the roles of CDH3 in cholangiocarcinoma, we investigated CDH3 function in HuCCT1 cells using specific siRNA. Transfection with CDH3 siRNA did not affect proliferation of HuCCT1 cells. However, cell migration and invasion were significantly reduced when CDH3 was down-regulated. In addition, expressions of several biomarkers for epithelial-mesenchymal transition (EMT) were not changed by CDH3 down-regulation. These results suggest that CDH3 regulates cell migration independent of EMT in cholangiocarcinoma cells.

Keywords

Acknowledgement

Supported by : Pusan National University Research Grant

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