The DOI matches its Crossref record; 14 of the 14 references it cites were found in a registry or an index.
A systems view of epithelial–mesenchymal transition signaling states
Open accessAbstract
Epithelial-mesenchymal transition (EMT) is an important contributor to the invasion and metastasis of epithelial-derived cancers. While considerable effort has focused in the regulators involved in the transition process, we have focused on consequences of EMT to prosurvival signaling. Changes in distinct metastable and 'epigentically-fixed' EMT states were measured by correlation of protein, phosphoprotein, phosphopeptide and RNA transcript abundance. The assembly of 1167 modulated components into functional systems or machines simplified biological understanding and increased prediction confidence highlighting four functional groups: cell adhesion and migration, metabolism, transcription nodes and proliferation/survival networks. A coordinate metabolic reduction in a cluster of 17 free-radical stress pathway components was observed and correlated with reduced glycolytic and increased oxidative phosphorylation enzyme capacity, consistent with reduced cell cycling and reduced need for macromolecular biosynthesis in the mesenchymal state. An attenuation of EGFR autophosphorylation and a switch from autocrine to paracrine-competent EGFR signaling was implicated in the enablement of tumor cell chemotaxis. A similar attenuation of IGF1R, MET and RON signaling with EMT was observed. In contrast, EMT increased prosurvival autocrine IL11/IL6-JAK2-STAT signaling, autocrine fibronectin-integrin α5β1 activation, autocrine Axl/Tyro3/PDGFR/FGFR RTK signaling and autocrine TGFβR signaling. A relatively uniform loss of polarity and cell-cell junction linkages to actin cytoskeleton and intermediate filaments was measured at a systems level. A more heterogeneous gain of ECM remodeling and associated with invasion and migration was observed. Correlation to stem cell, EMT, invasion and metastasis datasets revealed the greatest similarity with normal and cancerous breast stem cell populations, CD49f(hi)/EpCAM(-/lo) and CD44(hi)/CD24(lo), respectively.
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Cites
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“DNA binding is modulated by multiple proteins upregulated by EMT (FOSL2, ATF3, ARNTL, PHB and PHB2) [100].”
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Cited by
The epigenetics of epithelial-mesenchymal plasticity in cancer
Tam, W. L., & Weinberg, R. A. (2013) · Nature Medicine · doi:10.1038/nm.3336 · Cited by 1,163
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Epithelial-to-Mesenchymal Transition Rewires the Molecular Path to PI3K-Dependent Proliferation
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The multiverse nature of epithelial to mesenchymal transition
Simeone, P., Trerotola, M., Franck, J., Cardon, T., Marchisio, M., Fournier, I., Salzet, M., Maffia, M., & Vergara, D. (2019) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2018.11.004 · Cited by 98
Metadata
- Authors
- Thomson, S., Petti, F., Sujka-Kwok, I., Mercado, P., Bean, J., Monaghan, M., Seymour, S. L., Argast, G. M., Epstein, D. M., & Haley, J. D.
- Venue
- Clinical & Experimental Metastasis
- Published
- 2010-12-31
- Volume
- 28
- Issue
- 2
- Pages
- 137-155
- ISSN
- 0262-0898 (ISSN-L)
- 1573-7276
- OpenAlex
- W2022480285
- Cited by
- 211
- References
- 14
- FWCI
- 7.12
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Thomson, S., Petti, F., Sujka-Kwok, I., Mercado, P., Bean, J., Monaghan, M., Seymour, S. L., Argast, G. M., Epstein, D. M., & Haley, J. D. (2011). A systems view of epithelial–mesenchymal transition signaling states. Clinical & Experimental Metastasis. https://doi.org/10.1007/s10585-010-9367-3
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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