The transcription factor Snail controls epithelial–mesenchymal transitions by repressing E-cadherin expression

By A. Cano, Mirna Perez‐Moreno, I. Rodrigo, A. Locascio, M. Blanco, Marta G. Del Barrio, F. Portillo, M. Nieto. Nature Cell Biology, 2000

3,774 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology, Surgery

View Paper: https://www.semanticscholar.org/paper/4596fbec21a29a5e6473a76c04b3717da1b9a87b

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. M. Nieto
2. R. Weinberg
3. J. P. Thiery
4. Raghu Kalluri
5. Jing Yang
6. Thomas Brabletz
7. Youhua Liu
8. A. Cano

In Oncology

1. R. Weinberg
2. M. Nieto
3. Thomas Brabletz
4. Jing Yang
5. Raghu Kalluri
6. J. P. Thiery
7. E. Hay
8. Zena Werb

In Surgery

1. M. Nieto
2. Youhua Liu
3. Elaine Fuchs
4. J. P. Thiery
5. R. Weinberg
6. Eric R. Fearon
7. Raghu Kalluri
8. H. Acloque

Citations in the corpus

• The transcription factor Slug represses E-cadherin expression and induces epithelial to mesenchymal transitions: a comparison with Snail and E47 repressors (2003, methodology): “The generation of MDCK-Snailcells has been previously reported (Cano et al., 2000).”
• Ras and TGFβ cooperatively regulate epithelial cell plasticity and metastasis (2002, background): “cinoma cell lines (Cano et al., 2000).”
• Vitamin D3 promotes the differentiation of colon carcinoma cells by the induction of E-cadherin and the inhibition of β-catenin signaling (2001, background): “E-cadherin expression is inhibited by the product of Snail gene, which is a transcriptional repressor on the E-boxes located near the transcription start site (Batlle et al., 2000; Cano et al., 2000).”
• The protein kinase Akt induces epithelial mesenchymal transition and promotes enhanced motility and invasiveness of squamous cell carcinoma lines. (2003, background): “Indeed, SNAIL induces EMT by repressing E-cadherin transcription (4, 5).”
• The molecular mechanisms and therapeutic strategies of EMT in tumor progression and metastasis (2022, background): “The progression of EMT is regulated by the expression of EMT-translational factors (TFs) (such as SNAIL, ZEB, TWIST, and others) and miRNAs, as well as epigenetic and posttranslational regulators [10].”
• MicroRNAs in development and disease. (2011, background): “By targeting HMGA2, a chromatin remodeling protein, it suppresses the expression of Snail, which is expressed in metastatic tumors and has been implicated in the mechanism for EMT by directly suppressing E-cadherin (73).”
• Identification of conserved gene expression features between murine mammary carcinoma models and human breast tumors (2007, methodology): “Group II samples were derived from several models (2/10 Brca1Co/ Co;TgMMTV-Cre;p53+/-, 3/11 DMBA-induced, 1/5 p53-/transplant, 1/7 p53+/- IR, 1/10 TgMMTV-Neu and 1/7 TgWAP-T121) and also showed high expression of mesenchymal features (Figure 1g) that were shared with the normal samples in addition t”
• Dynamic EMT: a multi‐tool for tumor progression (2021, positive): “…to repress epithelial genes like the E-cadherin encoding gene CDH1 via binding to E-Box motifs in their cognate promoter regions (Nieto et al , 2016) as shown for SNAIL (Batlle et al , 2000; Cano et al , 2000), TWIST (Yang et al , 2004), ZEB1 (Eger et al , 2005), and ZEB2 (Comijn et al , 2001).”
• Correlation of Snail expression with histological grade and lymph node status in breast carcinomas (2002, background): “…that of E-cadherin, a direct correlation has been observed with the invasive and metastatic properties of mouse and human tumour cell lines derived from tissues such as skin, breast, colon, oral mucosa and melanoma (Batlle et al., 2000; Cano et al., 2000; Poser et al., 2001; Yokoyama et al., 2001).”
• Dual regulation of Snail by GSK-3β-mediated phosphorylation in control of epithelial–mesenchymal transition (2004, background): “Several transcription factors have been implicated in this repression, including zinc-finger proteins of the Snail/Slug famil”
• Epithelial–mesenchymal plasticity in carcinoma metastasis (2013, background): “During EMT, E-cadherin gene transcriptional repression (Batlle et al. 2000; Cano et al. 2000; Hajra et al. 2002), promoter methylation (Graff et al. 1995; Kanai et al. 1997; Saito et al. 1998), and protein phosphorylation and degradation (Zhou et al. 2004; Bachelder et al. 2005; Lester et al. 2007)…”
• Epithelial to mesenchymal transition in renal fibrogenesis: pathologic significance, molecular mechanism, and therapeutic intervention. (2004, background): “For instance, it is well known that E-cadherin suppression during carcinoma cell mesenchymal conversion is primarily mediated by Snail transcription factor (25,59,60), whereas its suppression in renal tubular epithelial cells during TGF- 1–induced EMT is clearly Snailindependent (32).”
• Induction of epithelial-mesenchymal transition in alveolar epithelial cells by transforming growth factor-beta1: potential role in idiopathic pulmonary fibrosis. (2005, background): “60 A recent study showed that decreases in expression of Nkx2.”