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González, B. ; Denzel, S.* ; Mack, B.* ; Conrad, M. ; Gires, O.

EpCAM is involved in maintenance of the murine embryonic stem cell phenotype.

Stem Cells 27, 1782-1791 (2009)
Epithelial cell adhesion molecule EpCAM is a transmembrane glycoprotein that is expressed on subsets of normal epithelia, numerous stem- and progenitor-type cells, and most carcinomas and highly overexpressed on cancer-initiating cells. The role of EpCAM in early development, particularly in stem-like cells, has remained unclear. Here, we show that the maintenance of self-renewal in murine embryonic stem (ES) cells depends on the high-level expression of EpCAM. Cultivation of ES cells under differentiation conditions in the absence of leukemia inhibitory factor (LIF) caused down-regulation of EpCAM along with decreased expression of cellular myelocytomatosis oncogene (c-Myc), Sex-determining region Y-Box 2, Octamer 3/4 (Oct3/4), and Stat3. As a consequence ES cells were morphologically differentiated and ceased to proliferate. RNA interference-mediated inhibition of EpCAM expression under self-renewal conditions resulted in quantitatively decreased proliferation, decreased Oct3/4, SSEA-1, and c-Myc expression, and diminished alkaline phosphatase activity. Conversely, exogenous expression of EpCAM partially compensated for the requirement of ES cells for LIF to retain a stem cell phenotype. Thus, murine EpCAM is a transmembrane protein, which is essential but by itself is not sufficient for maintenance of the ES cell phenotype.
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Publication type Article: Journal article
Document type Scientific Article
Keywords Cell adhesion molecules; Cell surface markers; Embryonic stem cells; Self-renewal; Antigen epcam; ep-cam; Self-renewal; Adhesion molecule; Breast-cancer; Expression; Carcinoma; Tumor; Differentiation; Proliferation
ISSN (print) / ISBN 0737-1454
e-ISSN 1549-4918
Journal Stem Cells
Quellenangaben Volume: 27, Issue: 8, Pages: 1782-1791 Article Number: , Supplement: ,
Publisher Wiley
Publishing Place Durham
Reviewing status Peer reviewed
Institute(s) CCG Molecular Oncology (AGV-KON)
Institute of Clinical Molecular Biology and Tumor Genetics (K.MOLBI)