EMT, the cytoskeleton, and cancer cell invasion
By Mahmut Yilmaz, Gerhard Christofori. Cancer Metastasis Review, 2009
1,811 citations recorded by the source corpus.
Subfields: Cell Biology, Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/5b9ef5f1d7966d635ca8761f43659539fa4f58aa
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In Cell Biology
- D. Hanahan
- R. Weinberg
- Harald Schuhwerk
- Thomas Brabletz
- Simone Brabletz
- Marc P. Stemmler
- Y. Yarden
- R. Derynck
In Molecular Biology
- R. Weinberg
- D. Hanahan
- Thomas Brabletz
- Simone Brabletz
- Samy Lamouille
- R. Derynck
- Marc P. Stemmler
- Yoko Katsuno
In Oncology
- R. Weinberg
- D. Hanahan
- Thomas Brabletz
- R. Derynck
- Simone Brabletz
- Samy Lamouille
- Yoko Katsuno
- Xiawei Wei
Citations in the corpus
- TGF-&bgr; signaling and epithelial–mesenchymal transition in cancer progression (2013, background): “Finally, the cells acquire invasive properties through increased expression and secretion of metalloproteases (MMPs), and cells that underwent EMT are also efficiently capable of synthesizing components of the ECM to reconstitute their microenvironment following cell invasion [15,18,19].”
- Hallmarks of cancer: the next generation. (2011, positive): “…become prominently implicated as a means by which transformed epithelial cells can acquire the abilities to invade, to resist apoptosis, and to disseminate (Klymkowsky and Savagner, 2009; Polyak and Weinberg, 2009; Thiery et al., 2009; Yilmaz and Christofori, 2009; Barrallo-Gimeno and Nieto, 2005).”
- The E-Cadherin and N-Cadherin Switch in Epithelial-to-Mesenchymal Transition: Signaling, Therapeutic Implications, and Challenges (2019, background): “During EMT, cleavage of E-cadherin leads to the destabilization of adherens junctions and the release of β-catenin to function as a transcriptional activator for cell proliferation [61,62].”
- Matrix Stiffness Modulates Proliferation, Chemotherapeutic Response and Dormancy in Hepatocellular Carcinoma Cells (2011, background): “During tumor dissemination, tumor cells are believed to acquire mesenchymal properties, enabling them to migrate through and invade surrounding tissues and enter the bloodstream (33).”
- Feedback regulation of EGFR signalling: decision making by early and delayed loops (2011, background): “One example of this late wave of fate-determining transcription is a process called the epithelial–mesenchymal transition (EMT”
- Mechanical stiffness grades metastatic potential in patient tumor cells and in cancer cell lines (2011, background): “The spread of cancer from its primary site to distant organs, the "invasion-metastasis cascade," is the main cause of cancer death and invasion of cells into the lymphatics and blood vessels is a crucial step in metastasis, correlating with a poorer patient prognosis (1).”
- EMT and tumor metastasis (2015, background): “Once at the plasma membrane, Ecadherin can also be inactivated by proteolytic cleavage or destabilized by phosphorylation of β-catenin [43].”
- Dynamic EMT: a multi‐tool for tumor progression (2021, positive): “To invade the surrounding tissues, e.g., TWIST or ZEB1 also induce the formation of invadopodia, specialized filopodia with proteolytic function (Yilmaz & Christofori, 2009; Eckert et al , 2011; Ridley, 2011; Sundararajan et al , 2015).”
- 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].”