A double-negative feedback loop between ZEB1-SIP1 and the microRNA-200 family regulates epithelial-mesenchymal transition.

By C. Bracken, P. A. Gregory, Natasha Kolesnikoff, A. Bert, Jun Wang, M. Shannon, Gregory J. Goodall. Cancer Research, 2008

1,089 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/322d6256d51f41ac0014b030a0e09ba9aeebf768

How researchers see this paper

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

In Cancer Research

1. Thomas Brabletz
2. Jing Yang
3. A. Lund
4. M. Jansson
5. Gianpiero di Leva
6. Yibin Kang
7. M. Garofalo
8. S. Piccolo

In Molecular Biology

1. Jing Yang
2. R. Weinberg
3. Thomas Brabletz
4. Simone Brabletz
5. A. Lund
6. Yibin Kang
7. M. Jansson
8. D. Medici

Citations in the corpus

• Dynamic EMT: a multi‐tool for tumor progression (2021, neutral): “Thus, the bidirectional transitions between EMT and MET states are potentiated by the ZEB/miR-200 circuit (Bracken et al , 2008; Burk et al , 2008; Wellner et al , 2009).”
• Epithelial-mesenchymal plasticity in cancer progression and metastasis (2019, background): “The miR-200 family of five miRNAs and miR-205 repress the expression of Zeb1/2 (Bracken et al., 2008; Burk et al., 2008; Gregory et al., 2008; Korpal et al., 2008; Park et al., 2008). miR-200s and Zeb1/2 form a double negative feedback loop where ZEB1/2 inhibits the expression of miR-200 miRNAs, and”
• TGF-&bgr; signaling and epithelial–mesenchymal transition in cancer progression (2013, background): “result, the ZEB1 and ZEB2 mRNA and protein levels are further increased and promote EMT responses [23].”
• Implications of the Hybrid Epithelial/Mesenchymal Phenotype in Metastasis (2015, background): “These components form two interlinked mutually inhibitory feedback loops – miR-34/SNAIL and miR-200/ZEB (26–28), such that EMT-inducing signals such as TGF β , EGF, HGF, and Notch activate ZEB and SNAIL, and p53 activates miR-200 and miR-34 (3) ( Figure 1B ).”
• The molecular mechanisms and therapeutic strategies of EMT in tumor progression and metastasis (2022, background): “It is widely known that the miR-200 family suppresses the production and activation of ZEB, which in turn suppresses the expression of miR-200 family [129].”
• CircNet: a database of circular RNAs derived from transcriptome sequencing data (2015, neutral): “The database is now publicly accessible at http: //circnet.mbc.nctu.edu.tw/.”
• Epithelial–mesenchymal plasticity in carcinoma metastasis (2013, background): “…(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 al. 2008; Burk et al. 2008; Gregory et al. 2008; Korpal and Kang 2008; Korpal et al. 2008; Park et al. 2008; Kim et al. 2011b).”
• Signaling mechanisms of the epithelial-mesenchymal transition (2014, background): “In turn, ZEB1 and ZEB2 bind to the E-box promoters ofmiR-200, creating a reciprocal feedback loop controlling EMT (51, 53).”
• MicroRNA and cancer (2012, background): “Likewise, the transcriptional repressor ZEB1 directly inhibits transcription of microRNA-200 family members miR- 141 and miR-200c, which in turn regulate both ZEB1 and ZEB2 (Bracken et al., 2008; Christoffersen et al., 2007), and strongly activate epithelial differentiation in pancreatic, colorectal”