Molecular mechanisms of epithelial–mesenchymal transition

By Samy Lamouille, Jian Xu, R. Derynck. Nature reviews. Molecular cell biology, 2014

7,497 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/815417a8834eb263821247c971b28eb9897a8bd8

How researchers see this paper

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

In Molecular Biology

In Oncology

Citations in the corpus

EMERGING BIOLOGICAL PRINCIPLES OF METASTASIS (2017, positive): “These complex programs are orchestrated and coordinated by a series of master EMT-inducing transcription factors (EMT-TFs), notably Snail, Slug, Twist and Zeb1, which have been explored in great experimental detail (De Craene and Berx, 2013; Lamouille et al., 2014).”
Revisiting the hallmarks of cancer. (2017, neutral): “Context-dependent (tissue- or tumor-specific) triggers include a number of growth factors [22], signaling pathways [109], tissue hypoxia [110], metabolic and mechanical stress, and matrix stiffness [111].”
Signaling mechanisms of the epithelial-mesenchymal transition (2014, background): “Adhesion to both the basement membrane and adjacent cells is critical for maintaining the epithelial phenotype (10).”
Targeting Epithelial–Mesenchymal Transition (EMT) to Overcome Drug Resistance in Cancer (2016, background): “Cells undergoing EMT display decreased expression level of epithelial genes (such as E-cadherin, ZO-1 and occludin) and increased expression level of mesenchymal g nes (such as N-cadherin, vimentin and fibronecti ) [7].”
The molecular mechanisms and therapeutic strategies of EMT in tumor progression and metastasis (2022, background): “The PAR complex defines the boundary between the basal and apical structural domains, while the Crumb complex is associated with the LIN-1 (PALS1) related protein (PALS1) and the PALS1associated tight junction (PATJ) complex, which controls apical structural domain formation [20, 36].”
Reciprocal regulation of TGF-β and reactive oxygen species: A perverse cycle for fibrosis (2015, neutral): “Signaling pathways including Smad, MAPK, and PI3K pathways are involved in the induction of EMT by TGF-β [231,232].”
TGF-β1 Signaling and Tissue Fibrosis. (2018, background): “More insight has emerged with greater usage of fibrotic human tissue samples for biomedical research, the development of novel techniques for genetic modifications to mice, and a greater understanding of some of the prominent EMT signaling pathways (Kalluri and Neilson 2003; Teng et al. 2007; Kallur”
EMT subtype influences epithelial plasticity and mode of cell migration (2018, methodology): “This process is often conceptualized as the end result of EMT leading to the dissemination of single tumor cells (Brabletz, 2012; Lamouille et al., 2014; Nieto et al., 2016; Savagner, 2015).”