Induction of EMT by twist proteins as a collateral effect of tumor-promoting inactivation of premature senescence.

By S. Ansieau, J. Bastid, A. Doreau, A. Morel, B. P. Bouchet, Clémence Thomas, Frédéric Fauvet, I. Puisieux, C. Doglioni, S. Piccinin and 6 more. Cancer Cell, 2008

752 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology, Physiology

View Paper: https://www.semanticscholar.org/paper/091e4e50dc3540bae4f314c258f5ca2d1f6b53e6

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In Molecular Biology

1. R. Weinberg
2. M. Nieto
3. Jing Yang
4. J. P. Thiery
5. Thomas Brabletz
6. Simone Brabletz
7. J. Tsai
8. R. Huang

In Oncology

1. R. Weinberg
2. M. Nieto
3. Thomas Brabletz
4. Jing Yang
5. J. P. Thiery
6. Simone Brabletz
7. R. Huang
8. J. Tsai

In Physiology

1. K. Polyak
2. R. Weinberg

Citations in the corpus

• Epithelial–mesenchymal plasticity in carcinoma metastasis (2013, background): “By inhibiting p53, Twist1 was able to cooperate with oncogenes such as Her2 and H-ras to promote malignant transformation (Valsesia-Wittmann et al. 2004; Ansieau et al. 2008; Morel et al. 2012; Piccinin et al. 2012), suggesting a potential role of EMT genes in tumor initiation.”
• Epithelial-mesenchymal transitions in development and disease. (2009, background): “Twist1 and Twist2 prevent cells from undergoing senescence induced by oncogenes by inhibiting p16/ink4a and p21/cip (Ansieau et al., 2008).”
• Transitions between epithelial and mesenchymal states: acquisition of malignant and stem cell traits (2009, background): “Furthermore, some of these transcription factors, including TWIST1, play a part in overcoming cellular senescenc”
• Epithelial-Mesenchymal Transition in Cancer: Parallels Between Normal Development and Tumor Progression (2010, background): “In addition to inducing a tumor-initiating cell phenotype, regulators of EMT also influence cell survival, specifically after treatment with chemotherapeutic agents [87, 88], as well as prevent oncogene-induced senescence [89], both properties associated with tumor progression.”
• Dynamic EMT: a multi‐tool for tumor progression (2021, neutral): “This mitigates oncogene-induced replication stress to overcome oncogene-induced senescence (OIS) in TP53 wild-type cells (Halazonetis et al , 2008) (Morel et al , 2017).”
• The ZEB/miR‐200 feedback loop—a motor of cellular plasticity in development and cancer? (2010, background): “…EuropEan MolEcular Biology organization4 that twist1 can override activated raS-induced senescence and can co operate for oncogenic transformation (ansieau et al, 2008). in addition, mouse embryonic fibroblasts from zEB1-null mice revealed proliferation defects and underwent premature…”
• MicroRNAs — the micro steering wheel of tumour metastases (2009, background): “; EMT is also a process crucial for tumour initiation, as shown by its requirement to bypass oncogene-induced cellular senescenc”
• The ins and outs of the epithelial to mesenchymal transition in health and disease. (2011, background): “The premature senescence triggered in response to Ras activation is also overcome when cells undergo the EMT (Ansieau et al. 2008, Liu et al. 2008).”