DeltaEF1 is a transcriptional repressor of E-cadherin and regulates epithelial plasticity in breast cancer cells

A. Eger; K. Aigner; S. Sonderegger; B. Dampier; S. Oehler; M. Schreiber; G. Berx; A. Cano; H. Beug; R. Foisner

doi:10.1038/sj.onc.1208429

DeltaEF1 is a transcriptional repressor of E-cadherin and regulates epithelial plasticity in breast cancer cells

A. Eger, K. Aigner, S. Sonderegger, B. Dampier, S. Oehler, M. Schreiber, G. Berx, A. Cano, H. Beug, R. Foisner

Institute Krems Bioanalytics

Research output: Contribution to journal › Article › peer-review

Abstract

Downregulation of E-cadherin is a crucial event for epithelial to mesenchymal transition (EMT) in embryonic development and cancer progression. Using the EpFosER mammary tumour model we show that during EMT, upregulation of the transcription al regulator deltaEF1 coincided with transcriptional repression of E-cadherin. Ectopic expression of deltaEF1 in epithelial cells was sufficient to downregulate E-cadherin and to induce EMT. Analysis of E-cadherin promoter activity and chromatin immunoprecipitation identified deltaEF1 as direct transcriptional repressor of E-cadherin. In human cancer cells, transcript levels of deltaEF1 correlated directly with the extent of E-cadherin repression and loss of the epithelial phenotype. The protein was enriched in nuclei of human cancer cells and physically associated with the E-cadherin promoter. RNA interference-mediated downregulation of deltaEF1 in cancer cells was sufficient to derepress E-cadherin expression and restore cell to cell adhesion, suggesting that deltaEF1 is a key player in late stage carcinogenesis. © 2005 Nature Publishing Group All rights reserved.

Original language	English
Pages (from-to)	2375-2385
Number of pages	11
Journal	Oncogene
Volume	24
Issue number	14
DOIs	https://doi.org/10.1038/sj.onc.1208429
Publication status	Published - 17 Jan 2005

Keywords

protein deltaEF1
repressor protein
unclassified drug
uvomorulin
cadherin
homeodomain protein
primer DNA
TCF8 protein
human
transcription factor
article
breast cancer
breast tumor
cancer growth
carcinogenesis
cell adhesion
cell transformation
controlled study
epithelium cell
human cell
immunoprecipitation
mesenchyme
phenotype
plasticity
priority journal
protein expression
RNA interference
transcription regulation
genetic transcription
genetics
metabolism
nucleotide sequence
pathology
physiology
promoter region
Base Sequence
Breast Neoplasms
Cadherins
DNA Primers
Epithelial Cells
Homeodomain Proteins
Humans
Promoter Regions (Genetics)
Repressor Proteins
Transcription Factors
Transcription
Genetic

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1038/sj.onc.1208429

https://www.scopus.com/inward/record.uri?eid=2-s2.0-20144388095&doi=10.1038%2fsj.onc.1208429&partnerID=40&md5=1dfa455057cd5819d322f57bfd07ffa7

Cite this

@article{887ddeff921f4a048f69697db77e1d17,

title = "DeltaEF1 is a transcriptional repressor of E-cadherin and regulates epithelial plasticity in breast cancer cells",

abstract = "Downregulation of E-cadherin is a crucial event for epithelial to mesenchymal transition (EMT) in embryonic development and cancer progression. Using the EpFosER mammary tumour model we show that during EMT, upregulation of the transcription al regulator deltaEF1 coincided with transcriptional repression of E-cadherin. Ectopic expression of deltaEF1 in epithelial cells was sufficient to downregulate E-cadherin and to induce EMT. Analysis of E-cadherin promoter activity and chromatin immunoprecipitation identified deltaEF1 as direct transcriptional repressor of E-cadherin. In human cancer cells, transcript levels of deltaEF1 correlated directly with the extent of E-cadherin repression and loss of the epithelial phenotype. The protein was enriched in nuclei of human cancer cells and physically associated with the E-cadherin promoter. RNA interference-mediated downregulation of deltaEF1 in cancer cells was sufficient to derepress E-cadherin expression and restore cell to cell adhesion, suggesting that deltaEF1 is a key player in late stage carcinogenesis. {\textcopyright} 2005 Nature Publishing Group All rights reserved.",

keywords = "protein deltaEF1, repressor protein, unclassified drug, uvomorulin, cadherin, homeodomain protein, primer DNA, TCF8 protein, human, transcription factor, article, breast cancer, breast tumor, cancer growth, carcinogenesis, cell adhesion, cell transformation, controlled study, epithelium cell, human cell, immunoprecipitation, mesenchyme, phenotype, plasticity, priority journal, protein expression, RNA interference, transcription regulation, genetic transcription, genetics, metabolism, nucleotide sequence, pathology, physiology, promoter region, Base Sequence, Breast Neoplasms, Cadherins, DNA Primers, Epithelial Cells, Homeodomain Proteins, Humans, Promoter Regions (Genetics), Repressor Proteins, Transcription Factors, Transcription, Genetic",

author = "A. Eger and K. Aigner and S. Sonderegger and B. Dampier and S. Oehler and M. Schreiber and G. Berx and A. Cano and H. Beug and R. Foisner",

note = "cited By 620",

year = "2005",

month = jan,

day = "17",

doi = "10.1038/sj.onc.1208429",

language = "English",

volume = "24",

pages = "2375--2385",

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TY - JOUR

T1 - DeltaEF1 is a transcriptional repressor of E-cadherin and regulates epithelial plasticity in breast cancer cells

AU - Eger, A.

AU - Aigner, K.

AU - Sonderegger, S.

AU - Dampier, B.

AU - Oehler, S.

AU - Schreiber, M.

AU - Berx, G.

AU - Cano, A.

AU - Beug, H.

AU - Foisner, R.

N1 - cited By 620

PY - 2005/1/17

Y1 - 2005/1/17

N2 - Downregulation of E-cadherin is a crucial event for epithelial to mesenchymal transition (EMT) in embryonic development and cancer progression. Using the EpFosER mammary tumour model we show that during EMT, upregulation of the transcription al regulator deltaEF1 coincided with transcriptional repression of E-cadherin. Ectopic expression of deltaEF1 in epithelial cells was sufficient to downregulate E-cadherin and to induce EMT. Analysis of E-cadherin promoter activity and chromatin immunoprecipitation identified deltaEF1 as direct transcriptional repressor of E-cadherin. In human cancer cells, transcript levels of deltaEF1 correlated directly with the extent of E-cadherin repression and loss of the epithelial phenotype. The protein was enriched in nuclei of human cancer cells and physically associated with the E-cadherin promoter. RNA interference-mediated downregulation of deltaEF1 in cancer cells was sufficient to derepress E-cadherin expression and restore cell to cell adhesion, suggesting that deltaEF1 is a key player in late stage carcinogenesis. © 2005 Nature Publishing Group All rights reserved.

AB - Downregulation of E-cadherin is a crucial event for epithelial to mesenchymal transition (EMT) in embryonic development and cancer progression. Using the EpFosER mammary tumour model we show that during EMT, upregulation of the transcription al regulator deltaEF1 coincided with transcriptional repression of E-cadherin. Ectopic expression of deltaEF1 in epithelial cells was sufficient to downregulate E-cadherin and to induce EMT. Analysis of E-cadherin promoter activity and chromatin immunoprecipitation identified deltaEF1 as direct transcriptional repressor of E-cadherin. In human cancer cells, transcript levels of deltaEF1 correlated directly with the extent of E-cadherin repression and loss of the epithelial phenotype. The protein was enriched in nuclei of human cancer cells and physically associated with the E-cadherin promoter. RNA interference-mediated downregulation of deltaEF1 in cancer cells was sufficient to derepress E-cadherin expression and restore cell to cell adhesion, suggesting that deltaEF1 is a key player in late stage carcinogenesis. © 2005 Nature Publishing Group All rights reserved.

KW - protein deltaEF1

KW - repressor protein

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KW - Promoter Regions (Genetics)

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U2 - 10.1038/sj.onc.1208429

DO - 10.1038/sj.onc.1208429

M3 - Article

SN - 0950-9232

VL - 24

SP - 2375

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JO - Oncogene

JF - Oncogene

IS - 14

ER -