ArticleJournal of cell science2016
PRL-3 disrupts epithelial architecture by altering the post-mitotic midbody position.
Article in Journal of cell science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
- Discovery of inhibitors of the cancer-promoting phosphatase PRL-3 and their evaluation in intestinal organoids.Bioorganic & medicinal chemistry · 2025Article
- PRL-3 as a metastasis-associated phosphatase in colorectal cancer: Mechanisms and therapeutic strategies.Clinical & experimental metastasis · 2025Review
- Modeling primary microcephaly with human brain organoids reveals fundamental roles of CIT kinase activity.The Journal of clinical investigation · 2024Article
- Soft Polyethylene Glycol Hydrogels Support Human PSC Pluripotency and Morphogenesis.ACS biomaterials science & engineering · 2024Article
- Phosphatase and Pseudo-Phosphatase Functions of Phosphatase of Regenerating Liver 3 (PRL-3) Are Insensitive to Divalent Metals In Vitro.ACS omega · 2023Article
- Article
- PRL-1/2 phosphatases control TRPM7 magnesium-dependent function to regulate cellular bioenergetics.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- E-cadherin mediates apical membrane initiation site localisation during de novo polarisation of epithelial cavities.The EMBO journal · 2022Article
- Apical-basal polarity and the control of epithelial form and function.Nature reviews. Molecular cell biology · 2022Review
- Won't You be My Neighbor: How Epithelial Cells Connect Together to Build Global Tissue Polarity.Frontiers in cell and developmental biology · 2022Review
- Cytokinetic Abscission Regulation in Neural Stem Cells and Tissue Development.Current stem cell reports · 2021Article
- The phosphatase PRL-3 affects intestinal homeostasis by altering the crypt cell composition.Journal of molecular medicine (Berlin, Germany) · 2021Article
- Induction of apically mistrafficked epiregulin disrupts epithelial polarity via aberrant EGFR signaling.Journal of cell science · 2021Article
- CD13 orients the apical-basal polarity axis necessary for lumen formation.Nature communications · 2021Article
- Cytokinetic abscission is part of the midblastula transition in early zebrafish embryogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Secreted midbody remnants are a class of extracellular vesicles molecularly distinct from exosomes and microparticles.Communications biology · 2021Article
- Phosphatase of regenerating liver-3 regulates cancer cell metabolism in multiple myeloma.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Actin-Membrane Release Initiates Cell Protrusions.Developmental cell · 2020Article
- Cytokinesis and postabscission midbody remnants are regulated during mammalian brain development.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Aurora B functions at the apical surface after specialized cytokinesis during morphogenesis inDevelopment (Cambridge, England) · 2020Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Disruption of epithelial architecture is a fundamental event during epithelial tumorigenesis. We show that the expression of the cancer-promoting phosphatase PRL-3 (PTP4A3), which is overexpressed in several epithelial cancers, in polarized epithelial MDCK and Caco2 cells leads to invasion and the formation of multiple ectopic, fully polarized lumens in cysts. Both processes disrupt epithelial architecture and are hallmarks of cancer. The pathological relevance of these findings is supported by the knockdown of endogenous PRL-3 in MCF-7 breast cancer cells grown in three-dimensional branched structures, showing the rescue from multiple-lumen- to single-lumen-containing branch ends. Mechanistically, it has been previously shown that ectopic lumens can arise from midbodies that have been mislocalized through the loss of mitotic spindle orientation or through the loss of asymmetric abscission. Here, we show that PRL-3 triggers ectopic lumen formation through midbody mispositioning without altering the spindle orientation or asymmetric abscission, instead, PRL-3 accelerates cytokinesis, suggesting that this process is an alternative new mechanism for ectopic lumen formation in MDCK cysts. The disruption of epithelial architecture by PRL-3 revealed here is a newly recognized mechanism for PRL-3-promoted cancer 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.