Diverse cellular and molecular mechanisms contribute to epithelial plasticity and metastasis

By S. Grünert, M. Jechlinger, H. Beug. Nature reviews. Molecular cell biology, 2003

725 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/134a5ec9e622880e825b5f15d7c0d1590d623535

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Citations in the corpus

Transcriptional regulation of cell polarity in EMT and cancer (2008, background): “Moreover, EMT can probably be considered as the most extreme manifestation of epithelial cell plasticity (Grünert et al., 2003; Huber et al., 2005; Scheel et al., 2007), and the appearance of the full EMT phenotype might be difficult to observe within tumours.”
NF-κB is essential for epithelial-mesenchymal transition and metastasis in a model of breast cancer progression (2004, background): “EMT also occurs during embryonic development and is regulated by an elaborate interplay of signaling pathways (12, 13, 15, 16).”
TGF-beta and the Smad signaling pathway support transcriptomic reprogramming during epithelial-mesenchymal cell transition. (2005, background): “EMT is also important during tumor progression by stimulating invasiveness and metastasis (Condeelis and Segall, 2003; Grünert et al., 2003).”
Epithelial to mesenchymal transition in renal fibrogenesis: pathologic significance, molecular mechanism, and therapeutic intervention. (2004, background): “Third, EMT is a dynamic, complicated process that may require the participation and integration of multiple signal pathways at different stages (25,26).”
TGF-β and epithelial-to-mesenchymal transitions (2005, background): “Vimentin expression has been suggested as a critical marker to distinguish ‘true, complete EMT’ from ‘cell scattering’ or ‘partial EMT’ (Janda et al., 2002a; Grunert et al., 2003).”
Distinct roles of Akt1 and Akt2 in regulating cell migration and epithelial–mesenchymal transition (2005, methodology): “ERK activation is enhanced by Akt1 down-regulation Hyperactivation of the ERK/MAP kinase pathway, via either activation of Ras or a growth factor receptor, plays a cooperative role in many models of EMT (for review see Grunert et al., 2003).”
Collective cell migration in morphogenesis, regeneration and cancer (2009, background): “This effect implicates E-cadherin as the dominant mediator of collective cell interactions, the loss of which may or may not be compensated for by other cell–cell adhesion pathway”
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].”
Epithelial-mesenchymal transition in cancer metastasis: mechanisms, markers and strategies to overcome drug resistance in the clinic. (2009, background): “These can express some but not all the EMT markers, result in a stable or transient EMT phenomenon and implicate a diversity of actors and pathways [109,208].”
New signals from the invasive front (2006, background): “During this process of epithelial–mesenchymal transition (EMT), cells progressively redistribute or downregulate their apical and basolateral epithelial-specific tight and adherens junction proteins (including E-cadherin and cytokeratins) and re-express mesenchymal molecules (including vimentin and ”
Epithelial-mesenchymal transitions: twist in development and metastasis. (2004, background): “Further studies including immuor phosphoinositide 3-kinase (PI3K) pathway, can po- nohistochemical detection of EMT master regulators like tently induce EMT in certain epithelial cells in culture Twist in the invasive front of human tumor samples may (Grunert et al., 2003; Thiery, 2002) (Figure 1).”
Epithelial-mesenchymal transition: at the crossroads of development and tumor metastasis. (2008, background): “In cultured MDCK epithelial cells, activation of the TGF-b/Smad pathway has been shown to coordinate with Ras activation to promote a full EMT phenotype (Grunert et al., 2003).”
A Mutant-p53/Smad complex opposes p63 to empower TGFbeta-induced metastasis. (2009, neutral): “A wealth of evidence in cancer cells and animal models clearly indicates that metastasis requires the combination of elevated TGFb and Ras signaling, but the mechanisms of this intersection remain unclear (Grunert et al., 2003).”