Cadherins and cancer: how does cadherin dysfunction promote tumor progression?

By Angela Jeanes, C. Gottardi, Alpha S. Yap. Oncogene, 2008

817 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/41c6d130c1c3148e60931c641b0901c632ce02fa

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In Molecular Biology

Citations in the corpus

Organizing the Cell Cortex: The role of ERM proteins (2010, result): “This is consistent with studies implicating ERMs in junctional remodelling and/or stability — processes known to be defective in tumour invasio”
E-cadherin mediates contact inhibition of proliferation through Hippo signaling-pathway components (2011, background): “Furthermore, Ecadherin also directly interacts with other effector proteins, including β-catenin, to inhibit its nuclear transport during Wnt signaling, and receptor tyrosine kinases to regulate their signaling activities (9).”
Involvement of members of the cadherin superfamily in cancer. (2009, background): “The possible functional implications, which were reviewed recently (Jeanes et al. 2008), include the sequestering of b-catenin in an E-cadherin-catenin adhesion complex (Fig.”
E-cadherin–integrin crosstalk in cancer invasion and metastasis (2013, background): “…in mouse models is not sufficient to activate b-catenin signalling (Herzig et al., 2007; Schackmann et al., 2011), and it appears likely that the ability of E-cadherin to bind b-catenin at the AJ leads to fine-tuning of signalling through the canonical Wnt–b-catenin pathway (Jeanes et al., 2008).”
Membrane fluctuations mediate lateral interaction between cadherin bonds (2017, background): “This selectivity is promoted by small variations in the two-dimensional binding affinity (2D-Ka) for trans-dimerization [3, 9], which allows proteins of the cadherin family to have a structural and regulatory role in tissue morphogenesis, homoeostasis [10] and malignancy: E-cadherins in particular s”
Transcriptional regulation of cell polarity in EMT and cancer (2008, background): “By contrast, overexpression of Par3 strongly blocked the EMTmediated effects of TGF-b treatment, including the downregulation of E-cadherin and a-smooth muscle actin expression (Wang et al., 2008).”
Epithelial-mesenchymal transition in cancer metastasis: mechanisms, markers and strategies to overcome drug resistance in the clinic. (2009, background): “As detailed earlier, the invasion-suppressor E-cadherin is a very important molecule in cancer progression and EMT induction [15,64].”