The transcription factor Slug represses E-cadherin expression and induces epithelial to mesenchymal transitions: a comparison with Snail and E47 repressors

By Victoria Bolós, H. Peinado, Mirna Perez‐Moreno, M. Fraga, Manel Esteller, A. Cano. Journal of Cell Science, 2003

1,191 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/90713b6c07248e838471264ec59cb96852fbc163

How researchers see this paper

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In Molecular Biology

1. R. Weinberg
2. M. Nieto
3. Thomas Brabletz
4. A. Cano
5. Simone Brabletz
6. H. Peinado
7. Manel Esteller
8. G. Berx

Citations in the corpus

• Up-regulation of miR-200 and let-7 by natural agents leads to the reversal of epithelial-mesenchymal transition in gemcitabine-resistant pancreatic cancer cells (2009, neutral): “Both ZEB1 and slug are transcription factors that repress the expression of E-cadherin (30, 31).”
• Epithelial-mesenchymal transitions: the importance of changing cell state in development and disease. (2009, neutral): “One consequence of the induction of EMT by Snail is the direct repression of E-cadherin expression (38–40), which, in turn, leads to the disruption of adherens junctions.”
• E-cadherin, β-catenin, and ZEB1 in malignant progression of cancer (2009, background): “members of the zinc finger homeobox (ZFH) family of repressors, ZEB1 and ZEB2 [3–14].”
• The Role of Snail in EMT and Tumorigenesis (2013, background): “Slug, another member of the Snail family of transcription factor, is known to be required for neural crest cell migration during development, has been characterized as strong E-cadherin repressor and major EMT inducer and is correlated with distant metastasis [84,85].”
• Cadherin switching (2008, background): “The expression of E-cadherin is negatively regulated by a number of zinc-finger-family transcription factors, including Snail, Slug, Twist, E12 (E47, TCFE2A), SIP1 (ZEB2) and EF1 (ZEB1), each of which has been reported to bind to the E-cadherin promoter to repress its transcription (Bolos et al., 20”
• Epithelial—mesenchymal and mesenchymal—epithelial transitions in carcinoma progression (2007, background): “Snail2, and other members of the Snail family such as Snail1, induce EMT by repressing the transcription of the key adherens junction protein E-cadherin (Batlle et al., 2000; Bolos et al., 2003).”
• Epithelial-mesenchymal transition in cancer metastasis: mechanisms, markers and strategies to overcome drug resistance in the clinic. (2009, background): “The first repressors to be identified were the zinc finger proteins SNAI1 (SNAIL) [74,76] and SNAI2 (SLUG) [77] and the Smad-interacting proteins ZEB1”
• Snail Mediates E-Cadherin Repression by the Recruitment of the Sin3A/Histone Deacetylase 1 (HDAC1)/HDAC2 Complex (2004, methodology): “a firefly luciferase reporter gene (10) was used to determine the activity of the”
• TGF-β and epithelial-to-mesenchymal transitions (2005, background): “…downmodulation (Savagner et al., 1997; Zavadil et al., 2001), ectopic expression of Slug results in repression of E-cadherin transcription via proximal E-box elements in the E-cadherin promoter and is sufficient to induce complete EMT in MDCK kidney cells (Hajra et al., 2002; Bolos et al., 2003).”