ArticleMolecular biology of the cell2014
Role of TGF-β receptor III localization in polarity and breast cancer progression.
Article in Molecular biology of the cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Exploring TGFBR3 in disease pathogenesis: Mechanisms, clinical implications, and pharmacological modulation.Journal of pharmaceutical analysis · 2026Review
- Proteoglycans in Breast Cancer: Friends and Foes.Biomolecules · 2025Review
- The Role of TGFBR3 in the Development of Lung Cancer.Protein and peptide letters · 2024Review
- ICAM1 promotes bone metastasis via integrin-mediated TGF-β/EMT signaling in triple-negative breast cancer.Cancer science · 2022Article
- Review
- A juxtamembrane basolateral targeting motif regulates signaling through a TGF-β pathway receptor in Drosophila.PLoS biology · 2022Article
- miR-19a and miR-424 target TGFBR3 to promote epithelial-to-mesenchymal transition and migration of tongue squamous cell carcinoma cells.Cell adhesion & migration · 2018Article
- A targeted transforming growth factor-beta (TGF-β) blocker, TTB, inhibits tumor growth and metastasis.Oncotarget · 2018Article
- Dually modified transmembrane proteoglycans in development and disease.Cytokine & growth factor reviews · 2018Review
- Basolateral delivery of the type I transforming growth factor beta receptor is mediated by a dominant-acting cytoplasmic motif.Molecular biology of the cell · 2017Article
- Altering the Proteoglycan State of Transforming Growth Factor β Type III Receptor (TβRIII)/Betaglycan Modulates Canonical Wnt/β-Catenin Signaling.The Journal of biological chemistry · 2016Article
- Signaling Receptors for TGF-β Family Members.Cold Spring Harbor perspectives in biology · 2016Review
- Mechanisms of TGFβ-Induced Epithelial-Mesenchymal Transition.Journal of clinical medicine · 2016Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The majority of breast cancers originate from the highly polarized luminal epithelial cells lining the breast ducts. However, cell polarity is often lost during breast cancer progression. The type III transforming growth factor-β cell surface receptor (TβRIII) functions as a suppressor of breast cancer progression and also regulates the process of epithelial-to-mesenchymal transition (EMT), a consequence of which is the loss of cell polarity. Many cell surface proteins exhibit polarized expression, being targeted specifically to the apical or basolateral domains. Here we demonstrate that TβRIII is basolaterally localized in polarized breast epithelial cells and that disruption of the basolateral targeting of TβRIII through a single amino acid mutation of proline 826 in the cytosolic domain results in global loss of cell polarity through enhanced EMT. In addition, the mistargeting of TβRIII results in enhanced proliferation, migration, and invasion in vitro and enhanced tumor formation and invasion in an in vivo mouse model of breast carcinoma. These results suggest that proper localization of TβRIII is critical for maintenance of epithelial cell polarity and phenotype and expand the mechanisms by which TβRIII prevents breast cancer initiation and progression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.