The DOI matches its Crossref record; 44 of the 44 references it cites were found in a registry or an index.
CD44 splice isoform switching in human and mouse epithelium is essential for epithelial-mesenchymal transition and breast cancer progression
Open accessAbstract
Epithelial-mesenchymal transition (EMT) is a tightly regulated process that is critical for embryogenesis but is abnormally activated during cancer metastasis and recurrence. Here we show that a switch in CD44 alternative splicing is required for EMT. Using both in vitro and in vivo systems, we have demonstrated a shift in CD44 expression from variant isoforms (CD44v) to the standard isoform (CD44s) during EMT. This isoform switch to CD44s was essential for cells to undergo EMT and was required for the formation of breast tumors that display EMT characteristics in mice. Mechanistically, the splicing factor epithelial splicing regulatory protein 1 (ESRP1) controlled the CD44 isoform switch and was critical for regulating the EMT phenotype. Additionally, the CD44s isoform activated Akt signaling, providing a mechanistic link to a key pathway that drives EMT. Finally, CD44s expression was upregulated in high-grade human breast tumors and was correlated with the level of the mesenchymal marker N-cadherin in these tumors. Together, our data suggest that regulation of CD44 alternative splicing causally contributes to EMT and breast cancer progression.
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The Epithelial-Mesenchymal Transition Generates Cells with Properties of Stem Cells
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Self-citationAlternative isoform regulation in human tissue transcriptomes
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Twist, a Master Regulator of Morphogenesis, Plays an Essential Role in Tumor Metastasis
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Self-citationSnail, Zeb and bHLH factors in tumour progression: An alliance against the epithelial phenotype?
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Self-citationCD44: From adhesion molecules to signalling regulators
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Cited by
Molecular mechanisms of epithelial–mesenchymal transition
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The biology and role of CD44 in cancer progression: Therapeutic implications
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Functional consequences of developmentally regulated alternative splicing
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Metadata
- Authors
- Brown, R. L., Reinke, L. M., Damerow, M. S., Perez, D., Chodosh, L. A., Yang, J., & Cheng, C.
- Venue
- Journal of Clinical Investigation
- Published
- 2011-03-01
- Volume
- 121
- Issue
- 3
- Pages
- 1064-1074
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W1997316363
- Cited by
- 631
- References
- 44
- FWCI
- 19.58
- Type
- journal article
- Language
- en
- Open access
- bronze
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- CoChat. (2026). Citation check: CD44 splice isoform switching in human and mouse epithelium is essential for epithelial-mesenchymal transition and breast cancer progression. https://app.cochat.ai/papers/10.1172/jci44540
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- Brown, R. L., Reinke, L. M., Damerow, M. S., Perez, D., Chodosh, L. A., Yang, J., & Cheng, C. (2011). CD44 splice isoform switching in human and mouse epithelium is essential for epithelial-mesenchymal transition and breast cancer progression. Journal of Clinical Investigation. https://doi.org/10.1172/jci44540
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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.
