Bmi1 is essential in Twist1-induced epithelial–mesenchymal transition
By Muh-Hwa Yang, Dennis Shin-Shian Hsu, Hsei-Wei Wang, Hsiao‐Jung Wang, Hsin-Yi Lan, Wen-Hao Yang, Chi-Hung Huang, S. Kao, C. Tzeng, S. Tai and 3 more. Nature Cell Biology, 2010
671 citations recorded by the source corpus.
Subfields: Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/393aaf35b4b1cc7052505a09c1eb3ec7332354f0
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Citations in the corpus
- The Cancer Stem Cell Niche: How Essential is the Niche in Regulating Stemness of Tumor Cells? (2015, neutral): “However, direct evidence showing a pro-metastatic role for these myeloid cells through immunosuppression is lacking, even though CD11b+Gr1+ and CD11b+Ly6G+ cells promote metastatic processes (Yang et al., 2010; Casbon et al., 2015).”
- The ins and outs of the epithelial to mesenchymal transition in health and disease. (2011, background): “Whether Twist belongs to one class or the other is still a matter of debate, as there is evidence for either an indirect action through Snail2 or direct repression when complexed with the polycomb-group protein BMI-1 (Casas et al. 2011, Yang et al. 2010).”
- Dynamic EMT: a multi‐tool for tumor progression (2021, neutral): “Similarly, in squamous cell carcinoma (SCC) TWIST is regulating BMI1 to cooperatively repress CDKN2A (p16 INK4A ) and promote tumor initiation capacities (Yang et al , 2010).”
- Epithelial-mesenchymal transitions: insights from development (2012, background): “Yang et al., 2010; Eckert et al., 2011 Srp and GATA Contains two GATA-type zinc fingers that bind to the consensus sequence AGATAG within regulatory regions.”
- The molecular mechanisms and therapeutic strategies of EMT in tumor progression and metastasis (2022, background): “It directly binds the Bmi1 promoter and activates Bmi1, and hence TWIST1 can upregulate BMI1.”
- Signaling mechanisms of the epithelial-mesenchymal transition (2014, background): “Regulation of transcription is not mediated by Twist1 alone; however, BMI1, a polycomb-group repressor complex protein, acts in a concerted fashion with Twist to repress E-cadherin and the cell cycle inhibitor p16INK4α (42).”