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Specific knockdown of Oct4 and beta 2-microglobulin expression by RNA interference in human embryonic stem cells and embryonic carcinoma cells
Author(s): Matin MM, Walsh JR, Gokhale PJ, Draper JS, Bahrami AR, Morton I, Moore HD, Andrews PW
Source: STEM CELLS    Volume: 22    Issue: 5    Pages: 659-668    Published: 2004  
Times Cited: 112     References: 26     
Abstract: We have used RNA interference (RNAi) to downregulate beta2-microglobulin and Oct4 in human embryonal carcinoma (hEC) cells and embryonic stem (hES) cells, demonstrating that RNAi is an effective tool for regulating specific gene activity in these human stem cells. The knockdown of Oct4 but not beta2-microglobulin expression in both EC and ES cells resulted in their differentiation, as indicated by a marked change in morphology, growth rate, and surface antigen phenotype, with respect to SSEA1, SSEA3, and TRA-1-60 expression. Expression of hCG and Gcm1 was also induced following knockdown of Oct4 expression, in both 2102Ep hEC cells and in H7 and H14 hES cells, consistent with the conclusion that, as in the mouse, Oct4 is required to maintain the undifferentiated stem cell state, and that differentiation to trophectoderm occurs in its absence. NTERA2 hEC cells also differentiated, but not to trophectoderm, suggesting their equivalence to a later stage of embryogenesis than other hEC and hES cells.
Document Type: Article
Language: English
Reprint Address: Andrews, PW (reprint author), Univ Sheffield, Ctr Stem Cell Biol, Western Bank, Sheffield S10 2TN, S Yorkshire England
Addresses:
1. Univ Sheffield, Ctr Stem Cell Biol, Sheffield S10 2TN, S Yorkshire England
2. Univ Sheffield, Dept Biomed Sci, Sheffield S10 2TN, S Yorkshire England
3. Axorida Ltd, Sheffield, S Yorkshire England
4. Univ Sheffield, Royal Hallamshire Hosp, Sect Reprod & Dev Med, Sheffield, S Yorkshire England
Publisher: ALPHAMED PRESS, ONE PRESTIGE PLACE, STE 290, MIAMISBURG, OH 45342-3758 USA
Subject Category: Biotechnology & Applied Microbiology; Oncology; Cell Biology; Hematology
IDS Number: 851FE
ISSN: 1066-5099
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