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Cited by 448

The DOI matches its Crossref record; 30 of the 30 references it cites were found in a registry or an index.

β-catenin/TCF4 complex induces the epithelial-to-mesenchymal transition (EMT)-activator ZEB1 to regulate tumor invasiveness

Open access
Sánchez-Tilló, Ester, de Barrios, Oriol, Siles, Laura, Cuatrecasas, Miriam, Castells, Antoni, Postigo, Antonio·2011·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.1108977108
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Abstract

In most carcinomas, invasion of malignant cells into surrounding tissues involves their molecular reprogramming as part of an epithelial-to-mesenchymal transition (EMT). Mutation of the APC gene in most colorectal carcinomas (CRCs) contributes to the nuclear translocation of the oncoprotein β-catenin that upon binding to T-cell and lymphoid enhancer (TCF-LEF) factors triggers an EMT and a proinvasive gene expression profile. A key inducer of EMT is the ZEB1 transcription factor whose expression promotes tumorigenesis and metastasis in carcinomas. As inhibitor of the epithelial phenotype, ZEB1 is never present in the epithelium of normal colon or the tumor center of CRCs where β-catenin remains membranous. We show here that ZEB1 is expressed by epithelial cells in intestinal tumors from human patients (familial adenomatous polyposis) and mouse models (APC Min/+ ) with germline mutations of APC that result in nuclear accumulation of β-catenin. However, ZEB1 is not expressed in the epithelium of hereditary forms of CRCs that carry wild-type APC and where β-catenin is excluded from the nucleus (Lynch syndrome). We found that β-catenin/TCF4 binds directly to the ZEB1 promoter and activates its transcription. Knockdown of β-catenin and TCF4 in APC -mutated CRC cells inhibited endogenous ZEB1, whereas forced translocation of β-catenin to the nucleus in APC -wild-type CRC cells induced de novo expression of ZEB1. Upregulation of MT1-MMP and LAMC2 by β-catenin/TCF4 has been linked to invasiveness in CRCs, and we show here that both proteins are activated by ZEB1 coexpressing with it in primary colorectal tumors with mutated APC . These results set ZEB1 as an effector of β-catenin/TCF4 signaling in EMT and tumor progression.

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Metadata

Authors
Sánchez-Tilló, E., de Barrios, O., Siles, L., Cuatrecasas, M., Castells, A., & Postigo, A.
Venue
Proceedings of the National Academy of Sciences
Publisher
Proceedings of the National Academy of Sciences
Published
2011-11-11
Volume
108
Issue
48
Pages
19204-19209
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
DOI
10.1073/pnas.1108977108
OpenAlex
W2050089891
Cited by
448
References
30
FWCI
9.52
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: β-catenin/TCF4 complex induces the epithelial-to-mesenchymal transition (EMT)-activator ZEB1 to regulate tumor invasiveness. https://app.cochat.ai/papers/10.1073/pnas.1108977108
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Sánchez-Tilló, E., de Barrios, O., Siles, L., Cuatrecasas, M., Castells, A., & Postigo, A. (2011). β-catenin/TCF4 complex induces the epithelial-to-mesenchymal transition (EMT)-activator ZEB1 to regulate tumor invasiveness. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.1108977108

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.