ArticleProceedings of the National Academy of Sciences of the United States of America2013
Transformation of polarized epithelial cells by apical mistrafficking of epiregulin.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 34 citations in OpenAlex.
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- Inflammatory, transcriptomic, and cell fate responses underlying the mammalian transmission of avian influenza viruses.Journal of virology · 2025Article
- Low-affinity ligands of the epidermal growth factor receptor are long-range signal transmitters in collective cell migration of epithelial cells.Cell reports · 2024Article
- A size filter at the Golgi regulates apical membrane protein sorting.Nature cell biology · 2024Article
- Inhibition of autocrine HGF maturation overcomes cetuximab resistance in colorectal cancer.Cellular and molecular life sciences : CMLS · 2024Article
- IGF2BP2 promotes cell invasion and epithelial-mesenchymal transition through Src-mediated upregulation of EREG in oral cancer.International journal of biological sciences · 2024Article
- Sequence and structural insights of monoleucine-based sorting motifs contained within the cytoplasmic domains of basolateral proteins.Frontiers in cell and developmental biology · 2024Review
- Cadherins and catenins in cancer: connecting cancer pathways and tumor microenvironment.Frontiers in cell and developmental biology · 2023Review
- Review
- The Role of EREG/EGFR Pathway in Tumor Progression.International journal of molecular sciences · 2021Review
- Induction of apically mistrafficked epiregulin disrupts epithelial polarity via aberrant EGFR signaling.Journal of cell science · 2021Article
- Polarized epidermal growth factor secretion ensures robust vulval cell fate specification inDevelopment (Cambridge, England) · 2020Article
- Protein kinase A-mediated phosphorylation of naked cuticle homolog 2 stimulates cell-surface delivery of transforming growth factor-α for epidermal growth factor receptor transactivation.Traffic (Copenhagen, Denmark) · 2019Article
- Broad-spectrum receptor tyrosine kinase inhibitors overcomeOncotarget · 2019Article
- Role of Epidermal Growth Factor Receptor (EGFR) and Its Ligands in Kidney Inflammation and Damage.Mediators of inflammation · 2018Review
- Muc1 knockout potentiates murine lung carcinogenesis involving an epiregulin-mediated EGFR activation feedback loop.Carcinogenesis · 2017Article
- Three-dimensional culture system identifies a new mode of cetuximab resistance and disease-relevant genes in colorectal cancer.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- The epidermal growth factor receptor pathway in chronic kidney diseases.Nature reviews. Nephrology · 2016Review
- EGF receptor ligands: recent advances.F1000Research · 2016Review
- Induction of lateral lumens through disruption of a monoleucine-based basolateral-sorting motif in betacellulin.Journal of cell science · 2015Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Establishment and maintenance of apico-basolateral trafficking pathways are critical to epithelial homeostasis. Loss of polarity and trafficking fidelity are thought to occur as a consequence of transformation; however, here we report that selective mistrafficking of the epidermal growth factor receptor (EGFR) ligand epiregulin (EREG) from the basolateral to the apical cell surface drives transformation. Normally, EREG is preferentially delivered to the basolateral surface of polarized Madin-Darby canine kidney cells. EREG basolateral trafficking is regulated by a conserved tyrosine-based basolateral sorting motif in its cytoplasmic domain (YXXΦ: Y(156)ERV). Both Y156 and V159 are required for basolateral sorting of EREG, because Y156A and V159G substitutions redirect EREG to the apical cell surface. We also show that basolateral sorting of EREG is adaptor protein 1B-independent. Apical mistrafficking of EREG has a distinctive phenotype. In contrast to transient EGFR tyrosine phosphorylation after basolateral EREG stimulation, apical EREG leads to prolonged EGFR tyrosine phosphorylation, which may be related, at least in part, to a lack of negative regulatory Y1045 phosphorylation and subsequent ubiquitylation. Notably, Madin-Darby canine kidney cells stably expressing apically mistrafficked EREG form significantly larger, hyperproliferative, poorly differentiated, and locally invasive tumors in nude mice compared with WT EREG-expressing cells.
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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.