Expression of Zeb1 in the differentiation of mouse embryonic stem cell

Embryonic stem cells (ESCs) differentiation is a process of replication and refinement, and the directional lineage differentiation of ESCs involves the epithelial-mesenchymal transition (EMT)- mesenchymal-epithelial transition (MET) process. A previous study revealed that Zinc finger E-box-binding...

Full description

Saved in:
Bibliographic Details
Published inOpen life sciences Vol. 17; no. 1; pp. 455 - 462
Main Authors Chen, Ting, Pan, Peng, Wei, Wei, Zhang, Yanmin, Cui, Guanghui, Yu, Zhendong, Guo, Xin
Format Journal Article
LanguageEnglish
Published Poland De Gruyter 09.05.2022
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Embryonic stem cells (ESCs) differentiation is a process of replication and refinement, and the directional lineage differentiation of ESCs involves the epithelial-mesenchymal transition (EMT)- mesenchymal-epithelial transition (MET) process. A previous study revealed that Zinc finger E-box-binding homeobox 1 (Zeb1) plays a vital role in EMT, which could repress E-cadherin promoter and induce an EMT in cells. To verify the expression of Zeb1 and its correlation with Lin28a in mouse ESCs differentiation, we performed qRT-PCR and western blots to detect the expression of Lin28a mRNA and protein after Zeb1 knockdown. The expression of Zeb1 decreased over time of mouse ESCs differentiation but significantly increased in mouse embryonal carcinoma cells. After knockdown of Zeb1, Lin28a and Vimentin expression were decreased, while E-cadherin expression increased both in mouse ESCs, EBs, GC1, and P19 cells. We found that Zeb1 promoted the invasive ability of mouse embryonal carcinoma cells. These results revealed that expression of Zeb1 decreased during the differentiation of ESCs, and Lin28a and EMT processes can be regulated by Zeb1, which need to be verified in the future studies.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
These authors have contributed equally to this work.
ISSN:2391-5412
2391-5412
DOI:10.1515/biol-2022-0042