ArticleMolecular & cellular proteomics : MCP2013
Phosphatase of regenerating liver 3 (PRL3) provokes a tyrosine phosphoproteome to drive prometastatic signal transduction.
Article in Molecular & cellular proteomics : MCP, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03191682 (A Phase I, First-in-Human Study of PRL3-ZUMAB In Advanced, Solid Tumors and Haematologic Malignancies), which is not on this map. Cited by 24 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.
A Phase I, First-in-Human Study of PRL3-ZUMAB In Advanced, Solid Tumors and Haematologic Malignancies
Who cites it
24 citing papers in PubMed, 33 citations in OpenAlex.
- Article
- The PRL2 phosphatase up-regulates miR-21 through activation of the JAK2/STAT3 pathway to down-regulate the PTEN tumor suppressor.The Biochemical journal · 2025Article
- The PACT Network: PRL, ARL, CNNM, and TRPM Proteins in Magnesium Transport and Disease.International journal of molecular sciences · 2025Review
- Deletion of PTP4A3 phosphatase in high-grade serous ovarian cancer cells decreases tumorigenicity and produces marked changes in intracellular signaling pathways and cytokine release.The Journal of pharmacology and experimental therapeutics · 2025Article
- Protein Tyrosine Phosphatase PRL-3: A Key Player in Cancer Signaling.Biomolecules · 2024Review
- A Phase I, First-in-Human Study of PRL3-zumab in Advanced, Refractory Solid Tumors and Hematological Malignancies.Targeted oncology · 2023Article
- Cisplatin or Doxorubicin Reduces Cell Viability via the PTPIVA3-JAK2-STAT3 Cascade in Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2023Article
- PRL3 as a therapeutic target for novel cancer immunotherapy in multiple cancer types.Theranostics · 2023Review
- Substrate-selective positive allosteric modulation of PTPRD's phosphatase by flavonols.Biochemical pharmacology · 2022Article
- Dual-Specificity Phosphatase 11 Is a Prognostic Biomarker of Intrahepatic Cholangiocarcinoma.Frontiers in oncology · 2021Article
- Protein tyrosine phosphatases: promising targets in pancreatic ductal adenocarcinoma.Cellular and molecular life sciences : CMLS · 2019Review
- Protein tyrosine phosphatase 4A3 (PTP4A3/PRL-3) promotes the aggressiveness of human uveal melanoma through dephosphorylation of CRMP2.Scientific reports · 2019Article
- A chemical genetics approach identifies PTP4A3 as a regulator of colon cancer cell adhesion.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Knockdown of PRL-3 increases mitochondrial superoxide anion production through transcriptional regulation of RAP1.Cancer management and research · 2018Article
- PRL-3 promotes telomere deprotection and chromosomal instability.Nucleic acids research · 2017Article
- Molecular Pathways: Targeting Protein Tyrosine Phosphatases in Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Review
- Antibody Array Revealed PRL-3 Affects Protein Phosphorylation and Cytokine Secretion.PloS one · 2017Article
- PRL3-zumab, a first-in-class humanized antibody for cancer therapy.JCI insight · 2016Article
- PRL-3 activates mTORC1 in Cancer Progression.Scientific reports · 2015Article
- Expression array analysis of the hepatocyte growth factor invasive program.Clinical & experimental metastasis · 2015Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Phosphatase of regenerating liver 3 (PRL3) is suspected to be a causative factor toward cellular metastasis when in excess. To date, the molecular basis for PRL3 function remains an enigma, making efforts at distilling a concerted mechanism for PRL3-mediated metastatic dissemination very difficult. We previously discovered that PRL3 expressing cells exhibit a pronounced increase in protein tyrosine phosphorylation. Here we take an unbiased mass spectrometry-based approach toward identifying the phosphoproteins exhibiting enhanced levels of tyrosine phosphorylation with a goal to define the "PRL3-mediated signaling network." Phosphoproteomic data support intracellular activation of an extensive signaling network normally governed by extracellular ligand-activated transmembrane growth factor, cytokine, and integrin receptors in the PRL3 cells. Additionally, data implicate the Src tyrosine kinase as the major intracellular kinase responsible for "hijacking" this network and provide strong evidence that aberrant Src activation is a major consequence of PRL3 overexpression. Importantly, the data support a PDGF(α/β)-, Eph (A2/B3/B4)-, and Integrin (β1/β5)-receptor array as being the predominant network coordinator in the PRL3 cells, corroborating a PRL3-induced mesenchymal-state. Within this network, we find that tyrosine phosphorylation is increased on a multitude of signaling effectors responsible for Rho-family GTPase, PI3K-Akt, STAT, and ERK activation, linking observations made by the field as a whole under Src as a primary signal transducer. Our phosphoproteomic data paint the most comprehensive picture to date of how PRL3 drives prometastatic molecular events through Src activation.
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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.