Molecular requirements for epithelial-mesenchymal transition during tumor progression.

By M. Huber, N. Kraut, H. Beug. Current Opinion in Cell Biology, 2005

1,846 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/d187eee4d1620f475478a304e298dbb08a1325b5

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Citations in the corpus

Targeting Epithelial–Mesenchymal Transition (EMT) to Overcome Drug Resistance in Cancer (2016, background): “These pathways are critical for CSC self-renewal and maintenance [42].”
Hypoxia promotes fibrogenesis in vivo via HIF-1 stimulation of epithelial-to-mesenchymal transition. (2007, background): “An important feature of transitioned epithelial cells is enhanced capacity for cell migration (31).”
Blockade of hedgehog signaling inhibits pancreatic cancer invasion and metastases: a new paradigm for combination therapy in solid cancers. (2007, background): “21), which, in turn, confers a greater invasive ability in cancer cells (20, 21).”
Wnt signaling: is the party in the nucleus? (2006, background): “Wnt signaling induces or stabilizes repressors of E-cadherin, such as Slug, Snail and Twist1, which mediate epithelial–mesenchymal transitions that are accompanied by changes in cell adhesion (Conacci-Sorrell et al. 2003) and mobility (for review, see Huber et al. 2005).”
Interplay of cadherin-mediated cell adhesion and canonical Wnt signaling. (2010, background): “It has been shown that the cellular context determines which pathways crosstalk to Snail, Slug, and Twist and regulate the expression of E-cadherin (reviewed by Nieto 2002; Huber et al. 2005).”
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”
A natural antisense transcript regulates Zeb2/Sip1 gene expression during Snail1-induced epithelial-mesenchymal transition. (2008, background): “Epithelial–mesenchymal transition (EMT) is a cellular process characterized by the loss of epithelial features and the acquisition of a mesenchymal phenotype (Thiery 2003; Huber et al. 2005).”
EMT, cancer stem cells and drug resistance: an emerging axis of evil in the war on cancer (2010, background): “This may mirror developmentally regulated EMT signaling pathways, such as Wnt, Notch and Hedgehog, which drive both normal and CSC renewal and maintenance (Huber et al., 2005; Malanchi et al., 2008; Peacock and Watkins, 2008).”
Epithelial-Mesenchymal Plasticity: A central regulator of cancer progression (2015, background): “A uthor M anuscript A uthor M anuscript A uthor M anuscript A uthor M anuscript metastatic dissemination (Huber et al., 2005; Morel et al., 2012; Rhim et al., 2012; Sarrio et al., 2008).”
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 ”
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).”