Loss of E-cadherin promotes metastasis via multiple downstream transcriptional pathways.

By T. Onder, Piyush B. Gupta, Sendurai A Mani, Jing Yang, Eric S. Lander, R. Weinberg. Cancer Research, 2008

1,539 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/20a0b62e51c4dad00206ebffebec095bd2168e6d

How researchers see this paper

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

In Molecular Biology

1. R. Weinberg
2. K. Guan
3. M. Nieto
4. Jing Yang
5. Thomas Brabletz
6. Simone Brabletz
7. J. P. Thiery
8. Bin Zhao

In Oncology

1. R. Weinberg
2. M. Nieto
3. Thomas Brabletz
4. Jing Yang
5. J. P. Thiery
6. Simone Brabletz
7. R. Huang
8. Tetsuo Noda

Citations in the corpus

• E-cadherin, β-catenin, and ZEB1 in malignant progression of cancer (2009, background): “expression caused upregulation of EMT associated transcriptional repressors, in particular ZEB1 and twist, suggesting a feed forward loop of E-cadherin repression [44].”
• Curcumin: A review of anti-cancer properties and therapeutic activity in head and neck squamous cell carcinoma (2011, positive): “increased tendency for tumor metastasis [174].”
• Cell detachment activates the Hippo pathway via cytoskeleton reorganization to induce anoikis. (2012, background): “YAP is known to induce epithelial–mesenchymal transition (EMT) (Overholtzer et al. 2006; Zhao et al. 2008), which has been shown to repress anoikis in mammary epithelial cells (Onder et al. 2008).”
• Direct Signaling Between Platelets and Cancer Cells Induces an Epithelial-Mesenchymal-Like Transition and Promotes Metastasis (2011, positive): “) ONDER_CDH1_TARGETS_2 MSigDB, (Onder et al., 2008) GIAMPIERI_TGFB (Giampieri et al.”
• E-cadherin–integrin crosstalk in cancer invasion and metastasis (2013, background): “…the downstream consequences of reduced E-cadherin functionality can impact on a number of other tumour-associated phenotypes, such as proliferation, survival, angiogenesis and colonization at metastatic sites (Derksen et al., 2006; Ma et al., 2010; Onder et al., 2008; Wendt et al., 2011).”
• Epithelial-mesenchymal transition: at the crossroads of development and tumor metastasis. (2008, background): “The EMT-inducing transcription factor Twist1 is overexpressed in two human cancer types, lobular breast carcinoma and diffused-type gastric cancer.”
• Transitions between epithelial and mesenchymal states: acquisition of malignant and stem cell traits (2009, background): “Multiple studies described differences between the mutational and epigenetic inactivation of epithelial cadherin ( E-cadherin ) in human breast carcinoma”
• Cadherins and cancer: how does cadherin dysfunction promote tumor progression? (2008, background): “Interestingly, the transcription factor Twist was recently observed to be upregulated when E-cadherin was depleted in cultured epithelial cells (Onder et al., 2008).”
• Identification of selective inhibitors of cancer stem cells by high-throughput screening (2009, methodology): “Confirming previous results, an shEcad vector triggered an EMT and resulted in acquisition of a mesenchymal phenotype (Figure 1A) (Onder et al., 2008).”
• Core epithelial-to-mesenchymal transition interactome gene-expression signature is associated with claudin-low and metaplastic breast cancer subtypes (2010, methodology): “Cells in which Ecadherin was experimentally down-regulated were also included in these analyses, as we previously demonstrated that this alteration could also serve to induce an EMT in these cells (24).”
• Interplay of cadherin-mediated cell adhesion and canonical Wnt signaling. (2010, background): “In other cases, loss of E-cadherin induces EMT without promoting b-catenin mobilization, but it affects other signaling pathways (see also Perrais et al. 2007; Onder et al. 2008).”
• Epithelial-mesenchymal transition in cancer metastasis: mechanisms, markers and strategies to overcome drug resistance in the clinic. (2009, background): “catenin appears to be mainly nuclear [57,108].”
• The E-Cadherin and N-Cadherin Switch in Epithelial-to-Mesenchymal Transition: Signaling, Therapeutic Implications, and Challenges (2019, background): “Loss of E-cadherin in cancer cells leads to metastatic dissemination and activation of several EMT transcription factors [24].”