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

By A. Eger, Kirsten Aigner, S. Sonderegger, B. Dampier, S. Oehler, M. Schreiber, G. Berx, A. Cano, H. Beug, R. Foisner. Oncogene, 2005

794 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/52118bf29bf62cc6c39cbd1ae0b305d453375c17

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Citations in the corpus

Epithelial–mesenchymal plasticity in carcinoma metastasis (2013, background): “…zinc finger E-box-binding homeobox family proteins Zeb1 and Zeb2, which are also able to suppress E-cadherin transcription (Comijn et al. 2001; Eger et al. 2005) via a double-negative feedback loop controlling Zeb1/Zeb2 and miRNA-200 family expression (Christoffersen et al. 2007; Bracken et…”
Involvement of members of the cadherin superfamily in cancer. (2009, background): “Knock-down of deltaEF1/ZEB1 in dedifferentiated human epithelial colon and breast cancer cell lines results in re-expression of E-cadherin and other epithelial differentiation markers (Eger et al. 2005; Spaderna et al. 2006; Spaderna et al. 2008).”
The transcription factor ZEB1 (δEF1) promotes tumour cell dedifferentiation by repressing master regulators of epithelial polarity (2007, methodology): “Cell culture and Affymetrix GeneChip analyses MDA-MB-231 and CAMA1 were cultivated as reported (Eger et al., 2005).”
Epithelial-mesenchymal plasticity in cancer progression and metastasis (2019, background): “Polycomb Complex 2 Is Required for E-cadherin Repression by the Snail1 Transcription Factor.”
MicroRNA function in cancer: oncogene or a tumor suppressor? (2009, background): “MiR-200c: DeltaEF1, a transcriptional repressor of Ecadherin, regulates epithelial plasticity in breast cancer cells [73].”
NF-κB represses E-cadherin expression and enhances epithelial to mesenchymal transition of mammary epithelial cells: potential involvement of ZEB-1 and ZEB-2 (2007, background): “Our preliminary RT–PCR analysis of RNA from primary breast cancers indicates ZEB-1 expression in primary breast cancer (data not shown), and previous studies have shown an inverse relationship between ZEB-1 and E-cadherin expression in breast cancer cell lines (Eger et al., 2005).”
Epithelial to mesenchymal transition is a determinant of sensitivity of non-small-cell lung carcinoma cell lines and xenografts to epidermal growth factor receptor inhibition. (2005, background): “The expression of Zeb-1 was recently shown to correlate with the degree of EMT in breast cancer cells ( 28 ), and E-cadherin has been shown to be highly regulated and repressed at the transcriptional level by factors including Snail, Slug, Twist, and ZEB (29, 30), likely requiring the recruitment of”
A double-negative feedback loop between ZEB1-SIP1 and the microRNA-200 family regulates epithelial-mesenchymal transition. (2008, background): “ZEB1 and SIP1 are directly implicated in the control of EMT (11, 12 ), a process underlain by characteristic changes in gene expression in which epithelial cells acquire mesenchymal characteristics.”
Loss of E-cadherin promotes metastasis via multiple downstream transcriptional pathways. (2008, background): “Interestingly, Twist and ZEB-1, both previously known to cause E-cadherin repression, were among the transcription factors up-regulated following E-cadherin loss (22, 44 ).”
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 miR-200 family determines the epithelial phenotype of cancer cells by targeting the E-cadherin repressors ZEB1 and ZEB2. (2008, background): “…1 [SIP1])—are important regulators in the complex network of transcriptional repressors that regulate the expression of E-cadherin and EMT through repression of a number of master regulators of epithelial polarity (Comijn et al. 2001; Eger et al. 2005; Aigner et al. 2007; Shirakihara et al. 2007).”
The miR-200 family and miR-205 regulate epithelial to mesenchymal transition by targeting ZEB1 and SIP1 (2008, background): “ZEB1 and SIP1 are repressors of E-cadherin transcription that have been implicated in EM”
A natural antisense transcript regulates Zeb2/Sip1 gene expression during Snail1-induced epithelial-mesenchymal transition. (2008, background): “Moreover, Snail1 induces the expression of the Zeb1 transcriptional factor (Guaita et al. 2002), a transcriptional repressor that also binds to E-cadherin promoter E-boxes (Grooteclaes and Frisch 2000; Eger et al. 2005).”