The DOI matches its Crossref record; 24 of the 24 references it cites were found in a registry or an index.
Transforming growth factor-β employs HMGA2 to elicit epithelial–mesenchymal transition
Open accessAbstract
Epithelial–mesenchymal transition (EMT) occurs during embryogenesis, carcinoma invasiveness, and metastasis and can be elicited by transforming growth factor-β (TGF-β) signaling via intracellular Smad transducers. The molecular mechanisms that control the onset of EMT remain largely unexplored. Transcriptomic analysis revealed that the high mobility group A2 (HMGA2) gene is induced by the Smad pathway during EMT. Endogenous HMGA2 mediates EMT by TGF-β, whereas ectopic HMGA2 causes irreversible EMT characterized by severe E-cadherin suppression. HMGA2 provides transcriptional input for the expression control of four known regulators of EMT, the zinc-finger proteins Snail and Slug, the basic helix-loop-helix protein Twist, and inhibitor of differentiation 2. We delineate a pathway that links TGF-β signaling to the control of epithelial differentiation via HMGA2 and a cohort of major regulators of tumor invasiveness and metastasis. This network of signaling/transcription factors that work sequentially to establish EMT suggests that combinatorial detection of these proteins could serve as a new tool for EMT analysis in cancer patients.
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1 retracted
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Self-citationRetractedTwist, a Master Regulator of Morphogenesis, Plays an Essential Role in Tumor Metastasis
Yang, J., Mani, S. A., Donaher, J. L., Ramaswamy, S., Itzykson, R. A., Come, C., Savagner, P., Gitelman, I., Richardson, A., & Weinberg, R. A. (2004) · Cell · doi:10.1016/j.cell.2004.06.006 · Cited by 3,855
TRANSFORMING GROWTH FACTOR-β REGULATION OF IMMUNE RESPONSES
Li, M. O., Wan, Y. Y., Sanjabi, S., Robertson, A.-K. L., & Flavell, R. A. (2006) · Annual Review of Immunology · doi:10.1146/annurev.immunol.24.021605.090737 · Cited by 2,206
SPECIFICITY AND VERSATILITY IN TGF-β SIGNALING THROUGH SMADS
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Molecular requirements for epithelial–mesenchymal transition during tumor progression
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Self-citationThe transcriptional repressor Snail promotes mammary tumor recurrence
Moody, S. E., Perez, D., Pan, T.-C., Sarkisian, C. J., Portocarrero, C. P., Sterner, C. J., Notorfrancesco, K. L., Cardiff, R. D., & Chodosh, L. A. (2005) · Cancer Cell · doi:10.1016/j.ccr.2005.07.009 · Cited by 750
The two faces of transforming growth factor β in carcinogenesis
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Integration of TGF‐β/Smad and Jagged1/Notch signalling in epithelial‐to‐mesenchymal transition
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Transforming Growth Factor β-1 Induces Snail Transcription Factor in Epithelial Cell Lines
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Cited by
Molecular mechanisms of epithelial–mesenchymal transition
Lamouille, S., Xu, J., & Derynck, R. (2014) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3758 · Cited by 8,091
Massagué, J. (2008) · Cell · doi:10.1016/j.cell.2008.07.001 · Cited by 3,907
Snail, Zeb and bHLH factors in tumour progression: An alliance against the epithelial phenotype?
Peinado, H., Olmeda, D., & Cano, A. (2007) · Nature reviews. Cancer · doi:10.1038/nrc2131 · Cited by 3,121
TGF-β-induced epithelial to mesenchymal transition
Xu, J., Lamouille, S., & Derynck, R. (2009) · Cell Research · doi:10.1038/cr.2009.5 · Cited by 2,804
EMT, cancer stem cells and drug resistance: an emerging axis of evil in the war on cancer
Singh, A., & Settleman, J. (2010) · Oncogene · doi:10.1038/onc.2010.215 · Cited by 2,545
Metadata
- Authors
- Thuault, S., Valcourt, U., Petersen, M., Manfioletti, G., Heldin, C.-H., & Moustakas, A.
- Venue
- The Journal of Cell Biology
- Publisher
- Rockefeller University Press
- Published
- 2006-07-10
- Volume
- 174
- Issue
- 2
- Pages
- 175-183
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- OpenAlex
- W2127690474
- Cited by
- 499
- References
- 24
- FWCI
- 8.84
- Type
- journal article
- Language
- en
- Open access
- green
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- Thuault, S., Valcourt, U., Petersen, M., Manfioletti, G., Heldin, C.-H., & Moustakas, A. (2006). Transforming growth factor-β employs HMGA2 to elicit epithelial–mesenchymal transition. The Journal of Cell Biology. https://doi.org/10.1083/jcb.200512110
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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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