Complex networks orchestrate epithelial–mesenchymal transitions

By J. P. Thiery, J. Sleeman. Nature reviews. Molecular cell biology, 2006

4,090 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/2c2ffc946fb39af45e75af9c01c3a97d7418f82b

How researchers see this paper

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

In Cell Biology

In Molecular Biology

In Oncology

Citations in the corpus

Cadherin switching (2008, background): “Here, we focus on transcriptional repression of E-cadherin, because this is the mechanism most likely to operate during cadherin switching, because E-cadherin transcriptional repressors have been implicated in EMT and the EMT-like changes seen in tumor cells are thought to be reversible (Thiery and ”
Reassessing epithelial to mesenchymal transition as a prerequisite for carcinoma invasion and metastasis. (2006, background): “1B) have been the subject of many reports and exhaustive reviews (18, 19).”
Exosomes in Cancer Development, Metastasis and Drug Resistance: A Comprehensive Review (2013, positive): “EMT, driven by a complex interaction network [170] is considered one of the hallmarks of aggressive tumors [171].”
A reciprocal repression between ZEB1 and members of the miR-200 family promotes EMT and invasion in cancer cells (2008, background): “EMBO open A reciprocal repression between ZEB1 and members of the miR-200 family promotes EMT and invasion in cancer cells”
Visualizing spatiotemporal dynamics of multicellular cell-cycle progression. (2008, background): “Monitoring Structural and Behavioral Changes and Cell-Cycle Dynamics of Cultured Cells The epithelial-mesenchymal transition (EMT) is a fundamental morphogenetic process by which mesenchymal cells are formed from epithelia during embryonic development, wound repair, and tumor progression in multicel”
A SNAIL1-SMAD3/4 transcriptional repressor complex promotes TGF-β mediated epithelial-mesenchymal transition (2009, neutral): “dtd" [ ]> Epithelial–mesenchymal transition (EMT) is essential for organogenesis and is triggered during carcinoma progression to an invasive stat”
The physics of cancer: the role of physical interactions and mechanical forces in metastasis (2011, neutral): “The role of EMT in cancer metastasis is being actively explore”
The ins and outs of the epithelial to mesenchymal transition in health and disease. (2011, background): “Baltimore: Williams & Wilkins Provides the first description of the reversibility of the EMT process: the MET.”
EMT, the cytoskeleton, and cancer cell invasion (2009, background): “This temporary and reversible phenomenon is known as the epithelial-mesenchymal transition (EMT), a process that is currently in the limelight of investigating the onset of cancer cell migration, invasion and metastatic dissemination [1, 2].”
The transcription factor ZEB1 (δEF1) promotes tumour cell dedifferentiation by repressing master regulators of epithelial polarity (2007, background): “EMT-inducing pathways, such as transforming growth factor-b (TGFb) and Wnt signalling trigger epithelial dedifferentiation by impairing the expression/ function of the epithelial adhesion protein E-cadherin (De Craene et al., 2005b; Thiery and Sleeman, 2006).”
Circulating tumor cells (CTC) detection: clinical impact and future directions. (2007, background): “As discussed previously, the most malignant CTC lose epithelial antigens (by EMT), which means that assays targeting epithelial cells in blood are susceptible to missing the detection of the most invasive tumor cells.”
Transcriptional regulation of cell polarity in EMT and cancer (2008, background): “To date, many different extracellular cues have been shown to trigger epithelial dedifferentiation and EMT, such as those involving transforming growth factor-b (TGF-b), Notch, fibroblast growth factor and Wnt signalling pathways (Barrallo-Gimeno and Nieto, 2005; De Craene et al., 2005a; Huber et al”