ArticleThe Journal of pharmacology and experimental therapeutics2010
Phosphatase of regenerating liver-1 promotes cell migration and invasion and regulates filamentous actin dynamics.
Article in The Journal of pharmacology and experimental therapeutics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The trial behind it
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- PTP4A2 Promotes Glioblastoma Progression and Macrophage Polarization under Microenvironmental Pressure.Cancer research communications · 2024Article
- PTP4A1 promotes oral squamous cell carcinoma (OSCC) metastasis through altered mitochondrial metabolic reprogramming.Cell death discovery · 2023Article
- PRL1 Promotes Glioblastoma Invasion and TumorigenesisFrontiers in oncology · 2021Article
- TheFrontiers in cellular and infection microbiology · 2021Article
- Enhanced PRL-1 expression in placenta-derived mesenchymal stem cells accelerates hepatic function via mitochondrial dynamics in a cirrhotic rat model.Stem cell research & therapy · 2020Article
- Paxillin promotes the migration and angiogenesis of HUVECs and affects angiogenesis in the mouse cornea.Experimental and therapeutic medicine · 2020Article
- Effect of Pharmacological Inhibition of the Catalytic Activity of Phosphatases of Regenerating Liver in Early T Cell Receptor Signaling Dynamics and IL-2 Production.International journal of molecular sciences · 2020Article
- Fast Diffusion Sustains Plasma Membrane Accumulation of Phosphatase of Regenerating Liver-1.Frontiers in cell and developmental biology · 2020Article
- Phosphatase of Regenerating Liver-1 (PRL-1) Regulates Actin Dynamics During Immunological Synapse Assembly and T Cell Effector Function.Frontiers in immunology · 2018Article
- Overexpression of PTP4A1 is associated with poor overall survival in non-small cell lung cancer.International journal of clinical and experimental pathology · 2018Article
- Migrastatics-Anti-metastatic and Anti-invasion Drugs: Promises and Challenges.Trends in cancer · 2017Review
- Simulated microgravity inhibits the migration of mesenchymal stem cells by remodeling actin cytoskeleton and increasing cell stiffness.Cytotechnology · 2016Article
- Article
- Suppression of cell migration is promoted by miR-944 through targeting of SIAH1 and PTP4A1 in breast cancer cells.BMC cancer · 2016Article
- Protein tyrosine phosphatase of liver regeneration-1 is required for normal timing of cell cycle progression during liver regeneration.American journal of physiology. Gastrointestinal and liver physiology · 2015Article
- Protein tyrosine phosphatases as potential therapeutic targets.Acta pharmacologica Sinica · 2014Review
- Phosphatase of regenerating liver: a novel target for cancer therapy.Expert opinion on therapeutic targets · 2014Review
- Integrated analysis of global mRNA and protein expression data in HEK293 cells overexpressing PRL-1.PloS one · 2013Article
- Tissue-specific alterations of PRL-1 and PRL-2 expression in cancer.American journal of translational research · 2012Article
- PRL-1 protein promotes ERK1/2 and RhoA protein activation through a non-canonical interaction with the Src homology 3 domain of p115 Rho GTPase-activating protein.The Journal of biological chemistry · 2011Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The phosphatases of regenerating liver (PRLs) are a unique family of plasma membrane-associated protein tyrosine phosphatases that have been hypothesized to be involved in metastatic cancer. How PRLs control cancer cell migration, invasion, and proliferation remains largely unknown. In the current study, we demonstrate a role for PRL-1 in the regulation of filamentous actin dynamics, which could promote cell metastatic processes. Human A549 non-small-cell lung cancer cells stably expressing wild-type PRL-1 exhibited a 60% increase in migration and a 3-fold increase in invasion. Cells expressing catalytic mutants of PRL-1 (C104S and D72A) lacked increased cell migration and invasion, indicating that these phenotypic changes required PRL-1 phosphatase activity. In contrast, PRL-1 small interfering RNA decreased in vitro lung cancer cell migration and invasion. The cadherin-catenin complex and dynamic filamentous actin are believed to control cellular invasiveness. Expression of wild-type PRL-1, but not phosphatase-inactive PRL-1 (C104S or D72A), decreased E-cadherin, vinculin, and paxillin expression. Ectopic expression of wild-type PRL-1 increased RhoA levels, which have an important role in actin filament assembly and stabilization of focal adhesion, and decreased activated Cdc42 and Rac. The Rho-associated protein kinase inhibitor, (R)-(+)-trans-4-(1-aminoethyl)-N-(4-pyridyl) cyclohexanecarboxamide dihydrochloride (Y-27632), decreased RhoA activity, actin filament levels, and cellular migration and invasion in PRL-1-expressing cells. These results suggest that PRL-1 could be a productive cancer therapeutic target and support further efforts to identify its substrates.
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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.