miR-34 and SNAIL form a double-negative feedback loop to regulate epithelial-mesenchymal transitions
By Helge Siemens, R. Jackstadt, Sabine Hünten, Markus Kaller, A. Menssen, U. Götz, H. Hermeking. Cell Cycle, 2011
626 citations recorded by the source corpus.
Subfields: Cancer Research, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/0989df99c42ffe432321333c2ca3677c8d339546
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In Cancer Research
- Thomas Brabletz
- M. Nieto
- Yibin Kang
- Harald Schuhwerk
- Simone Brabletz
- Marc P. Stemmler
- F. Greten
- H. Hermeking
In Molecular Biology
- Thomas Brabletz
- M. Nieto
- Yibin Kang
- Simone Brabletz
- Marc P. Stemmler
- Wei Dang Lu
- Harald Schuhwerk
- F. Greten
Citations in the corpus
- IL-6R/STAT3/miR-34a feedback loop promotes EMT-mediated colorectal cancer invasion and metastasis. (2014, methodology): “Furthermore, we and others have recently shown that SNAIL, another well-established inducer of EMT, is a direct target of miR-34a (18, 19).”
- Epithelial Plasticity: A Common Theme in Embryonic and Cancer Cells (2013, background): “Double-negative feedback loops have been described between EMT-TFs (Snail, Zeb and Gata3 factors) and several miRs, including members of the miR-200 family and miR-34a (48-50), which promote MET and protect the epithelial phenotype (Figure 4).”
- Epithelial–mesenchymal plasticity in carcinoma metastasis (2013, neutral): “4; Kim et al. 2011a; Siemens et al. 2011).”
- Epithelial-mesenchymal plasticity in cancer progression and metastasis (2019, background): “The expression of SNAI1 can be similarly repressed by miR-34 (Siemens et al., 2011), miR-203 (Moes et al.”
- Dynamic EMT: a multi‐tool for tumor progression (2021, positive): “Similar to the ZEB/miR-200 negative feedback loop, SNAIL and the miR-34 family constitute additional epithelial plasticity regulatory loops (Siemens et al , 2011; Diaz-Lopez et al , 2014) (Fig 1B).”
- Mathematical Modelling of Molecular Pathways Enabling Tumour Cell Invasion and Migration (2015, background): “Gene expression of E-cadherin is inhibited by the transcription factors Snai1/2, Zeb1/2 and Twist1, while gene expression of Ncadherin (cdh2) is induced by the same transcription factors [8,10,11].”