TGF-β downregulates E-cadherin expression via a novel ZEB1-dependent mechanism

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ID: 320539
2026
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Abstract
Abstract Zinc finger E-box-binding homeobox 1 (ZEB1) is a core transcription factor regulating epithelial-mesenchymal transition (EMT), and its high expression is associated with malignant cancer phenotypes and a poor prognosis. ZEB1 mediates downregulation of E-cadherin (encoded by CDH1), as a hallmark of cells undergoing EMT. We previously identified two distinct modes of E-cadherin downregulation by ZEB1, namely, basal repression and stimulus-dependent repression. The current study aimed to investigate the mechanisms responsible for stimulus-dependent repression induced by transforming growth factor-β (TGF-β), using ZEB1-knockout cells. Knockout of ZEB1 resulted in upregulation of basal E-cadherin expression and attenuation of its downregulation following TGF-β treatment. TGF-β-induced E-cadherin downregulation required Smad3 signaling, but did not accompany upregulation of ZEB1 expression, suggesting functional modulation of ZEB1. C-terminal binding proteins were required for basal repression but not for TGF-β-induced downregulation. Consistently, basal repression of CDH1 by ZEB1, but not TGF-β-induced downregulation, was accompanied by histone deacetylation in the CDH1 regulatory regions; however, both of these processes required histone deacetylase activity. Histone deacetylase may therefore play a role in regulating the expression/function of factor(s) required for TGF-β-induced CDH1 downregulation. These results suggest that TGF-β downregulates E-cadherin expression via a novel ZEB1-dependent mechanism.
Reference Key
openalex_W7167969651 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Shigeo Otake, Yuka Itoh, Masao Saitoh, Keiji Miyazawa
Journal The Journal of Biochemistry
Year 2026
DOI
10.1093/jb/mvag052
URL
https://doi.org/10.1093/jb/mvag052
Keywords Keywords not found

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