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Please use this identifier to cite or link to this item: http://ntour.ntou.edu.tw:8080/ir/handle/987654321/17866

Title: 上皮細胞附著因子(EpCAM)與緊密結合蛋白因子(tight junction protein claudin-7)於反程序化老鼠成體細胞為誘導型全分化潛能幹細胞時所扮演的角色
Roles of EpCAM and CLDN-7 in reprogramming mouse fibroblast into induced pluripotent stem cells
Authors: Yao-De Huang
黃耀德
Contributors: NTOU:Institute of Bioscience and Biotechnology
國立臺灣海洋大學:生物科技研究所
Keywords: 全分化潛能幹細胞
EpCAM
Date: 2010
Issue Date: 2011-07-04
Abstract: 上皮細胞黏附因子(Epithelial cell adhesion molecule,EpCAM)是一種細胞表面蛋白分子,在許多的癌症細胞表現,並具有引發癌症的潛能。其被蛋白脢剪切後,釋放其胞內部份EpICD (EpCAM intracellular domain),進而活化 c-Myc (C terminal myelocytomatosis oncogene) 的表現。此外,EpCAM與緊密連結蛋白中的CLDN-7 (Claudin-7) 所形成的複合體則會促進腫瘤形成與發育。我們觀察到在老鼠胚胎幹細胞(mouse embyronic stem cells,mES)與經由反程序化而形成之誘導型多分化潛能幹細胞(induced pluripotent stem cell,iPS)皆會表現EpCAM及CLDN-7。且EpCAM與CLDN-7會隨著反程序化的過程而逐漸活化表現。而大量表現EpCAM及EpICD則會提高誘導型多分化潛能幹細胞的形成效率,再者,CLDN-7可以協同EpCAM增進誘導型多分化潛能幹細胞的產率。反之,抑制EpCAM及CLDN-7的表現則會降低誘導型多分化潛能幹細胞的產率。然而,在已分化之體細胞(老鼠纖維母細胞)中單獨表現EpCAM或CLDN-7並無法活化多分化潛能基因之表現。我們的研究結果顯示,EpCAM可以正向調控反程序化的效率,但其調控機制則需更進一步的研究。
Epithelial cell adhesion molecule (EpCAM) is a cell adhesion molecule and a potential target for therapeutic antibodies. Recently, EpCAM has been shown to regulate tumor cell proliferation by its nucleocytoplasmic intracellular domain fragment (ICD). EpCAM intracellular domain (EpICD) activates C terminal myelocytomatosis oncogene (c-Myc) in nucleus by Wnt signal pathway. On the other hand, the complex of EpCAM and the tight junction protein claudin-7 (CLDN-7) would promote tumorigenicity and accelerates tumor growth. We observed that EpCAM and CLDN-7 express in both mouse embryonic stem cells and induced poluripotent stem cells. In this study we first discovered that the expressions of EpCAM and CLDN-7 would be activated when reprogramming mouse embryonic fibroblast cells into induced pluripotent stem cells. The efficiency of iPS reprogramming was enhanced by overexpressing EpCAM, CLDN-7 or both. Furthermore, silence of endogenous EpCAM or CLDN-7 resulted in the reduction of iPS reprogramming. However, ectopic expression of EpCAM and CLDN-7 in differential somatic cells such as mouse fibroblast cells had no effect on the activation of pluripotency-associated gene Nanog, Oct4, Sox2, c-Myc and KLF4. Our data show that EpCAM positively regulates iPS reprogramming, yet the detail mechanism remains unclear.
URI: http://ethesys.lib.ntou.edu.tw/cdrfb3/record/#G0M97360014
http://ntour.ntou.edu.tw/ir/handle/987654321/17866
Appears in Collections:[生命科學暨生物科技學系] 博碩士論文

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