ArticlePloS one2013
Src-mediated phosphorylation of the tyrosine phosphatase PRL-3 is required for PRL-3 promotion of Rho activation, motility and invasion.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
26 citing papers in PubMed, 38 citations in OpenAlex.
- Article
- Phosphatases of regenerating liver downregulate PTEN to promote tumorigenesis.Biochemical Society transactions · 2026Review
- ZebrafishInternational journal of molecular sciences · 2026Article
- The PACT Network: PRL, ARL, CNNM, and TRPM Proteins in Magnesium Transport and Disease.International journal of molecular sciences · 2025Review
- Biomarkers of lymph node metastasis in colorectal cancer: update.Frontiers in oncology · 2024Review
- Emerging Role of Plant-Based Dietary Components in Post-Translational Modifications Associated with Colorectal Cancer.Life (Basel, Switzerland) · 2023Review
- Cisplatin or Doxorubicin Reduces Cell Viability via the PTPIVA3-JAK2-STAT3 Cascade in Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2023Article
- Anti-PRL-3 Monoclonal Antibody inhibits the Growth and Metastasis of colorectal adenocarcinoma.Journal of Cancer · 2023Article
- PRL3 as a therapeutic target for novel cancer immunotherapy in multiple cancer types.Theranostics · 2023Review
- Protein Tyrosine Phosphatases: Mechanisms in Cancer.International journal of molecular sciences · 2021Review
- Dual-Specificity Phosphatase 11 Is a Prognostic Biomarker of Intrahepatic Cholangiocarcinoma.Frontiers in oncology · 2021Article
- Review
- Regulation of Src Family Kinases during Colorectal Cancer Development and Its Clinical Implications.Cancers · 2020Review
- Protein tyrosine phosphatases: promising targets in pancreatic ductal adenocarcinoma.Cellular and molecular life sciences : CMLS · 2019Review
- Review
- Critical relevance of genomic gains of PRL-3/EGFR/c-myc pathway genes in liver metastasis of colorectal cancer.Oncology letters · 2019Article
- The tuberous sclerosis complex subunit TBC1D7 is stabilized by Akt phosphorylation-mediated 14-3-3 binding.The Journal of biological chemistry · 2018Article
- Targeting ovarian cancer and endothelium with an allosteric PTP4A3 phosphatase inhibitor.Oncotarget · 2018Article
- Molecular Pathways: Targeting Protein Tyrosine Phosphatases in Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Review
- Regulatory mechanisms of phosphatase of regenerating liver (PRL)-3.Biochemical Society transactions · 2016Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The metastasis-associated tyrosine phosphatase PRL-3/PTP4A is upregulated in numerous cancers, but the mechanisms modulating PRL-3 activity other than its expression levels have not been investigated. Here we report evidence for both Src-dependent tyrosine phosphorylation of PRL-3 and Src-mediated regulation of PRL-3 biological activities. We used structural mutants, pharmacological inhibitors and siRNA to demonstrate Src-dependent phosphorylation of endogenous PRL-3 in SW480 colon cancer cells. We also demonstrated that PRL-3 was not tyrosine phosphorylated in SYF mouse embryo fibroblasts deficient in Src, Yes and Fyn unless Src was re-expressed. Further, we show that platelet-derived growth factor (PDGF) can stimulate PRL-3 phosphorylation in a Src-dependent manner. Finally, we show that PRL-3-induced cell motility, Matrigel invasion and activation of the cytoskeleton-regulating small GTPase RhoC were abrogated in the presence of the phosphodeficient PRL-3 mutant Y53F, or by use of a Src inhibitor. Thus, PRL-3 requires the activity of a Src kinase, likely Src itself, to promote these cancer-associated phenotypes. Our data establish a model for the regulation of PRL-3 by Src that supports the possibility of their coordinate roles in signaling pathways promoting invasion and metastasis, and supports simultaneous use of novel molecularly targeted therapeutics directed at these proteins.
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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.