The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.
Paracrine and Autocrine Signals Induce and Maintain Mesenchymal and Stem Cell States in the Breast
Open accessAbstract
Summary The epithelial-mesenchymal transition (EMT) has been associated with the acquisition of motility, invasiveness and self-renewal traits. During both normal development and tumor pathogenesis this change in cell phenotype is induced by contextual signals that epithelial cells receive from their microenvironment. The signals that are responsible for inducing an EMT and maintaining the resulting cellular state have been unclear. We describe three signaling pathways, involving Transforming Growth Factor (TGF)-β as well as canonical and non-canonical Wnt signaling, that collaborate to induce activation of the EMT program and thereafter function in an autocrine fashion to maintain the resulting mesenchymal state. Downregulation of endogenously synthesized inhibitors of autocrine signals in epithelial cells enables the induction of the EMT program. Conversely, disruption of autocrine signaling by added inhibitors of these pathways inhibits migration and self-renewal in primary mammary epithelial cells, and inhibits tumorigenicity and metastasis by their transformed derivatives.
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Cites
Cluster analysis and display of genome-wide expression patterns
Eisen, M. B., Spellman, P. T., Brown, P. O., & Botstein, D. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.25.14863 · Cited by 16,184
Smyth, G. K. (2004) · Statistical Applications in Genetics and Molecular Biology · doi:10.2202/1544-6115.1027 · Cited by 11,829
Zebrafish Prickle, a Modulator of Noncanonical Wnt/Fz Signaling, Regulates Gastrulation Movements
Veeman, M. T., Slusarski, D. C., Kaykas, A., Louie, S. H., & Moon, R. T. (2003) · Current Biology · doi:10.1016/s0960-9822(03)00240-9 · Cited by 945
Human breast cancer cells generated by oncogenic transformation of primary mammary epithelial cells
Elenbaas, B., Spirio, L., Koerner, F., Fleming, M. D., Zimonjic, D. B., Donaher, J. L., Popescu, N. C., Hahn, W. C., & Weinberg, R. A. (2001) · Genes & Development · doi:10.1101/gad.828901 · Cited by 878
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Cited by
New insights into the mechanisms of epithelial–mesenchymal transition and implications for cancer
Dongre, A., & Weinberg, R. A. (2019) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-018-0080-4 · Cited by 3,876
Self-citationEMT, CSCs, and drug resistance: the mechanistic link and clinical implications
Shibue, T., & Weinberg, R. A. (2017) · Nature Reviews Clinical Oncology · doi:10.1038/nrclinonc.2017.44 · Cited by 2,539
Self-citationThe Cancer Stem Cell Niche: How Essential Is the Niche in Regulating Stemness of Tumor Cells?
Plaks, V., Kong, N., & Werb, Z. (2015) · Cell Stem Cell · doi:10.1016/j.stem.2015.02.015 · Cited by 1,557
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
Self-citationTackling the cancer stem cells — what challenges do they pose?
Pattabiraman, D. R., & Weinberg, R. A. (2014) · Nature Reviews Drug Discovery · doi:10.1038/nrd4253 · Cited by 990
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Metadata
- Authors
- Scheel, C., Eaton, E. N., Li, S. H.-J., Chaffer, C. L., Reinhardt, F., Kah, K.-J., Bell, G., Guo, W., Rubin, J., Richardson, A. L., & Weinberg, R. A.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2011-06
- Volume
- 145
- Issue
- 6
- Pages
- 926-940
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W2164618834
- Cited by
- 858
- References
- 4
- FWCI
- 39.84
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Scheel, C., Eaton, E. N., Li, S. H.-J., Chaffer, C. L., Reinhardt, F., Kah, K.-J., Bell, G., Guo, W., Rubin, J., Richardson, A. L., & Weinberg, R. A. (2011). Paracrine and Autocrine Signals Induce and Maintain Mesenchymal and Stem Cell States in the Breast. Cell. https://doi.org/10.1016/j.cell.2011.04.029
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.