E2F transcription factor 1 (E2F1) enhances the proliferation, invasion and EMT of trophoblast cells by binding to Zinc Finger E-Box Binding Homeobox 1 (ZEB1).
Bioengineered
; 13(2): 2360-2370, 2022 02.
Article
em En
| MEDLINE
| ID: mdl-35030974
ABSTRACT
Preeclampsia (PE) is a serious pregnancy syndrome, which is mainly caused by attenuated trophoblast proliferation and invasion. It has been verified that E2F transcription factor 1 (E2F1) is lowly expressed in PE. It is identified that E2F1 binds to the promoter region of Zinc Finger E-Box Binding Homeobox 1 (ZEB1) in JASPAR datasets. ZEB1 is also a transforming factor that can facilitate EMT. The present work was designed to investigate the biological functions of E2F1 and ZEB1 on the proliferation, invasiveness and EMT of trophoblast cells and further explore the molecular mechanism underlying the participation of E2F1 and ZEB1 in the behaviors of trophoblast cells. Results revealed that upregulation of E2F1 reinforced the proliferation, invasiveness and EMT of trophoblast cells and downregulation of E2F1 exhibited opposite effects on trophoblast proliferation, invasion and EMT. It was confirmed that E2F1 bound to the promoter region of ZEB1 and two binding sites (E1 and E2) in ZEB1 promoter region to E2F1 was identified by CHIP assays. Luciferase reporter assay further verified the binding relationship between E2F1 and ZEB1. Overexpression of ZEB1 rescued the suppressing effects of E2F1 knockdown on proliferation, invasiveness and EMT of trophoblast cells. To conclude, E2F1 could promote trophoblast proliferation and invasion and strengthen EMT of trophoblast cells by enhancing ZEB1 expression.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Trofoblastos
/
Proliferação de Células
/
Fator de Transcrição E2F1
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Transição Epitelial-Mesenquimal
/
Homeobox 1 de Ligação a E-box em Dedo de Zinco
Tipo de estudo:
Prognostic_studies
Limite:
Humans
Idioma:
En
Revista:
Bioengineered
Ano de publicação:
2022
Tipo de documento:
Article
País de afiliação:
China