Epithelial Plasticity: A Common Theme in Embryonic and Cancer Cells

By M. Nieto. Science, 2013

944 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/e3580d2f0a115d9999a961722f6a15eeebc7eec5

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Citations in the corpus

Epithelial-Mesenchymal Plasticity: A central regulator of cancer progression (2015, background): “Once activated, continued expression of an EMT program within a carcinoma cell may depend on continuous paracrine signals received from the stroma; such dependence dictates that carcinoma cells will lapse back into an epithelial state (via an MET) when they no longer experience these inductive signa”
The basics of epithelial–mesenchymal transition (EMT): A study from a structure, dynamics, and functional perspective (2019, background): “…adhesion and increased motility, through which they cross barrier and migrates towards long distances owing to intense alternations in their cytoskeleton structural design (Sotiriou et al., 2003, Thiery & Lim, 2013; Kalluri & Weinberg, 2009; Mittal, 2018; Nieto, 2013; Sarrio et al., 2008).”
Signaling mechanisms of the epithelial-mesenchymal transition (2014, background): “In the embryo, multiple rounds of EMT and MET are necessary to complete gastrulation and primitive streak formation, highlighting the reversibility of this process (16).”
The RNA binding protein quaking regulates formation of circRNAs. (2015, positive): “This has parallels in vivo as exemplified by the reversals of EMT that occur in some tissues during embryological development, while reversible plasticity is thought to play an important role in metastatic colonization (Brabletz, 2012; Nieto, 2013).”
Metastatic Stem Cells: Sources, Niches, and Vital Pathways (2014, background): “E-box binding factor), Twist, and others (Nieto, 2013).”
Regulation of epithelial-mesenchymal transition through epigenetic and post-translational modifications (2016, background): “EMT has been classified into three categories: type I, type II and type III [17, 18].”
Epithelial–mesenchymal transition in tumor metastasis (2016, background): “The hallmarks of the EMT program are loss of adherence junctions and apical–basal polarity, acquisition of mesenchymal phenotype, and gain of motility and invasion (Nieto, 2013).”
Implications of the Hybrid Epithelial/Mesenchymal Phenotype in Metastasis (2015, background): “Importantly, EMT and MET, whether in physiological or pathological contexts, are not binary processes (5, 6).”
EMT and tumor metastasis (2015, background): “More recently, the role of adherent EMT in pathogenesis of fibrosis and metastasis of certain carcinogenic tumors has been described [1-13].”