演題抄録

International Session(Poster)

開催概要
開催回
第51回・2013年・京都
 

Rab11 Up-regulated E-cadherin to Induce Cell Transformation in Colon Carcinoma

演題番号 : ISP-15

[筆頭演者]
Yuan-Chiang Chung:1 
[共同演者]
King-Jen Chang:1、Wei-Ting Chao:2

1:Department of Sugery, Cheng Ching General Hospital,Chung-Kang Br.,Taiwan、2:Department of Life Science,Tunghai Univ.,Taiwan

 

Background. In most epithelial cell-based cancers like colorectal cancer, epithelial mesenchymal transition (EMT) is thought to be a marker of tumor progression. In the process of EMT, the disassembly of junctional adhesion complexes such as E-cadherin and catenin is a remarkable sign during changes in cell morphology and polarity. However, E-cadherin expression is dynamic, and is regulated by the cellular endocytic system; it is also involved in cell signaling mechanisms. Therefore, E-cadherin may have varying functions in tumor progression. In this study, we investigated the role of E-cadherin in colorectal tumors and the relationship with recycling endosome protein Rab11 in colon cell transformation. Methods. For tissue screening, the expressions of E-cadherin and Rab11 in colorectal tumors were identified by immunohistochemistry. For the in vitro cell biology experiment, GFP-tagged Rab11 plasmid was transfected into HT29 colon cells, and the E-cadherin expression and cell transformation were monitored by Western blot and confocal microscopy.Results. Proportionally increased E-cadherin and Rab11 were observed in most of the colorectal tumor tissues. When GFP-tagged Rab11 plasmid was overexpressed in cultured colon cell line HT-29, the E-cadherin expression was up-regulated, and a fibroblast-like cell polarity was induced, which resulted in cell transformation. Conclusion. This study demonstrated the importance of the overexpression of Rab11 and E-cadherin in colorectal cancer. Therefore, Rab11 together with E-cadherin could be potential markers for colorectal cancer progression and therapy.

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