Cell adhesion and signalling by cadherins and Ig-CAMs in cancer

By U. Cavallaro, Gerhard Christofori. Nature Reviews. Cancer, 2004

1,377 citations recorded by the source corpus.

Subfields: Cell Biology, Cellular and Molecular Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/cff75ebe8f1a07b62c384b349ff8827473bb0e96

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Citations in the corpus

The molecular mechanisms and therapeutic strategies of EMT in tumor progression and metastasis (2022, background): “The roles of EMT and MET in tumor metastasis During the process of cell detachment from in situ, the downregulation or degradation of E-cadherin and the upregulation of N-cadherin destabilize AJs and disrupt the intercellular junctions of MCSCs, promoting cell migration and invasion [29, 159].”
Ovarian cancer development and metastasis. (2010, background): “One of the molecules critical for the adhesion of neighboring epithelial cells is E-cadherin, a membrane glycoprotein located at cell adherens junctions.(42,43) Ecadherin connects through - and -catenin to the actin microfilaments within the cytoplasm, thereby anchoring epithelial cells to each othe”
Trp53R172H and KrasG12D cooperate to promote chromosomal instability and widely metastatic pancreatic ductal adenocarcinoma in mice. (2005, background): “Loss of E cadherin expression has been implicated in the epithelial-to-mesenchymal transition (EMT) thought to precede the development of an invasive and metastatic phenotype, perhaps by altering critical interactions in a structured epithelium (Cavallaro and Christofori, 2004).”
Glutamine and cancer: cell biology, physiology, and clinical opportunities. (2013, positive): “Loss of the epithelial cell-cell adhesion molecule E-cadherin is a component of the epithelial-mesenchymal transition, and is sufficient to induce migration, invasion, and tumor progression (33, 34).”
Notch signaling mediates hypoxia-induced tumor cell migration and invasion (2008, background): “The E-cadherin promoter is repressed by several transcriptional repressors (8), including the zinc finger transcription factor Snail-1 (9); for review, see ref.”
The epithelial–mesenchymal transition: new insights in signaling, development, and disease (2006, neutral): “Loss of E-cadherin is a hallmark of metastatic carcinoma (Cavallaro and Christofori, 2004), and proteomic analysis of breast cancer reveals that circulating mammary tumor cells, or those found as micrometastases, show evidence of mesenchymal conversion (Willipinski-Stapelfeldt et al.”
Recent advances in three‐dimensional multicellular spheroid culture for biomedical research (2008, background): “Signal transduction might be initiated through the βcatenin complex [10], eventually leading to differentiated characteristics observed in MCS.”
DeltaEF1 is a transcriptional repressor of E-cadherin and regulates epithelial plasticity in breast cancer cells (2005, background): “DeltaEF1 represses E-cadherin in human breast cancer cells Loss of E-cadherin expression in human tumours is frequently associated with poor prognosis and survival, most likely due to enhanced invasiveness and metastasis (Cavallaro and Christofori, 2004).”
Hallmarks of cancer: the next generation. (2011, positive): “The frequently observed downregulation and occasional mutational inactivation of E-cadherin in human carcinomas provided strong support for its role as a key suppressor of this hallmark capability (Berx and van Roy, 2009; Cavallaro and Christofori, 2004).”
Significance analysis of functional categories in gene expression studies: a structured permutation approach (2005, background): “We note that the role of nuclear transport in cancer (Kau et al., 2004) and cancer aggressiveness (Agudo et al.”
E-cadherin, β-catenin, and ZEB1 in malignant progression of cancer (2009, background): “involved in E-cadherin associated signaling refer to the review of Cavallaro and Christofori [41].”
Defining the Role of Hypoxia-Inducible Factor 1 in Cancer Biology and Therapeutics (2009, neutral): “For example, loss of E-cadherin expression is essential for cancer cell invasion and metastasis (Cavallaro and Christofori, 2004).”