The role of βigh3 in human esophageal carcinoma cells and relationship with epithelial-mesenchymal transition

碩士 === 國立陽明大學 === 生命科學暨基因體科學研究所 === 98 === Transforming growth factor-β-induced gene-human clone 3 (βigh3) is an extracellular matrix protein which can bind to integrins, fibronectin and several types of collagen through FAS1 domain and RGD domain. In many human cancers, the level of βigh3 mRNA was...

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Bibliographic Details
Main Authors: Jui-Ting Chien, 簡瑞庭
Other Authors: Fen-Hwa Wong
Format: Others
Language:zh-TW
Published: 2010
Online Access:http://ndltd.ncl.edu.tw/handle/61490674198726319329
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Summary:碩士 === 國立陽明大學 === 生命科學暨基因體科學研究所 === 98 === Transforming growth factor-β-induced gene-human clone 3 (βigh3) is an extracellular matrix protein which can bind to integrins, fibronectin and several types of collagen through FAS1 domain and RGD domain. In many human cancers, the level of βigh3 mRNA was up-regulated. It has been reported that βigh3 binds to integrins to regulate cell migration, adhesion and proliferation in different cell types. However, some studies have indicated that βigh3 functions as a tumor suppressor. So, the real function of βigh3 is still unclear. In our laboratory, we have shown that βigh3 mRNA was over-expressed in human esophageal carcinoma tissues. In order to understand the function of βigh3 in esophageal carcinoma cells, we knockdown βigh3 gene expression in TE-9 cells by shRNA. The βigh3-knockdown cells increased expression of mesenchymal markers : Vimentin, N-cadherin and Twist, and had fibroblast-like morphology and loose cell-cell junction. In addition, knockdown βigh3 in TE-9 cells promoted cell migration and invasive ability. Moreover, we also found βigh3-knockdown cells had higher anchorage independent growth ability than control cells. According to these data, βigh3 seems suppress cell migration, invasion and anchorage independent growth through inhibition of epithelial-mesenchymal tansition (EMT) in esophageal carcinoma cells. However, the possible mechanisms and signal pathways that involved in βigh3-regulated EMT are unclear, and need further investigation.