The SLUG zinc-finger protein represses E-cadherin in breast cancer.

By K. M. Hajra, David Y. Chen, Eric R. Fearon. Cancer Research, 2002

1,050 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/cd39231c21e5a75888fb3690738ef4c0d81f16b4

How researchers see this paper

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

Citations in the corpus

Snail Mediates E-Cadherin Repression by the Recruitment of the Sin3A/Histone Deacetylase 1 (HDAC1)/HDAC2 Complex (2004, background): “An additional member of the Snail family, Slug, has also been reported to act as an E-cadherin repressor (10, 22).”
Epithelial-mesenchymal transition: at the crossroads of development and tumor metastasis. (2008, background): “…transcription, thereby causing the dissolution of cell-cell adhesion that occurs during EMT; these include Slug, a close relative of Snail (Hajra et al., 2002), and two members of the ZEB family of transcription factors, ZEB1 (dEF1) (Eger et al., 2005) and ZEB2 (SIP1) (Comijn et al.,…”
Interplay of cadherin-mediated cell adhesion and canonical Wnt signaling. (2010, background): “Both Snail and Slug bind to the E-box motive of the E-cadherin promoter through a carboxy-terminal zink-finger domain and suppress the expression of E-cadherin (Batlle et al. 2000; Cano et al. 2000; Hajra et al. 2002; Bolos et al. 2003).”
Repression of E-cadherin by the polycomb group protein EZH2 in cancer (2008, methodology): “…repression by snail and slug, ubiquitination and degradation of the E-cadherin and lysosomal targeting of the E-cadherin for degradation (Batlle et al., 2000; Fujita et al., 2002; Hajra et al., 2002; Peinado et al., 2004; Saito et al., 2004; Takeno et al., 2004; Palacios et al., 2005).”
Spatiotemporal regulation of epithelial-mesenchymal transition is essential for squamous cell carcinoma metastasis. (2012, background): “The EMT program is orchestrated through a network of transcription factors, including Twist1 (Yang et al., 2004), Snail1/2 (Batlle et al., 2000; Cano et al., 2000; Hajra et al., 2002), Zeb1/2 (Comijn et al., 2001; Eger et al., 2005), and FOXC2 (Mani et al., 2007).”
The transcription factor Slug represses E-cadherin expression and induces epithelial to mesenchymal transitions: a comparison with Snail and E47 repressors (2003, result): “These data are also in agreement with a recent report indicating that Slug is a repressor of E-cadherin in breast carcinoma cell lines (Hajra et al., 2002).”
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)…”
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”
Somatic inactivation of E-cadherin and p53 in mice leads to metastatic lobular mammary carcinoma through induction of anoikis resistance and angiogenesis. (2006, background): “…that several transcription repressors of E-cadherin, such as SIP1, Snail, Slug, and Twist (Savagner et al., 1997; Batlle et al., 2000; Cano et al., 2000; Comijn et al., 2001; Hajra et al., 2002; Yang et al., 2004) can induce epithelial-to-mesenchymal transition (EMT) and subsequent metastasis.”
ISMARA: automated modeling of genomic signals as a democracy of regulatory motifs (2014, unknown): “transcription factors[70] and by ZEB1[71].”