ArticleThe Journal of clinical investigation2013
Metastasis-associated PRL-3 induces EGFR activation and addiction in cancer cells.
Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 56 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.
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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
56 citing papers in PubMed, 85 citations in OpenAlex.
- A randomized, open-label, two-cycle, two-crossover phase I clinical trial comparing the bioequivalence and safety of afatinib and GiotrifJournal of cancer research and clinical oncology · 2023Trial
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- PTP4A3 dephosphorylates EGFR to promote metastasis and enhance sensitivity to lapatinib in hepatocellular carcinoma.Oncogene · 2026Article
- Phosphatases of regenerating liver downregulate PTEN to promote tumorigenesis.Biochemical Society transactions · 2026Review
- PRL-3 as a metastasis-associated phosphatase in colorectal cancer: Mechanisms and therapeutic strategies.Clinical & experimental metastasis · 2025Review
- Targeting of PTP4A3 overexpression sensitises HGSOC cells towards chemotherapeutic drugs.Molecular oncology · 2025Article
- From Tyrosine Kinases to Tyrosine Phosphatases: New Therapeutic Targets in Cancers and Beyond.Pharmaceutics · 2024Review
- Protein Tyrosine Phosphatase PRL-3: A Key Player in Cancer Signaling.Biomolecules · 2024Review
- PRL1 and PRL3 promote macropinocytosis via its lipid phosphatase activity.Theranostics · 2024Article
- Exploiting frequent and specific expression of PRL3 in pediatric solid tumors for first-in-child use of PRL3-zumab humanized antibody.Molecular therapy oncolytics · 2023Article
- Metastasis organotropism in colorectal cancer: advancing toward innovative therapies.Journal of translational medicine · 2023Review
- A Phase I, First-in-Human Study of PRL3-zumab in Advanced, Refractory Solid Tumors and Hematological Malignancies.Targeted oncology · 2023Article
- Exosomes as crucial emerging tools for intercellular communication with therapeutic potential in ovarian cancer.Future science OA · 2023Review
- Article
- PRL3 as a therapeutic target for novel cancer immunotherapy in multiple cancer types.Theranostics · 2023Review
- CEMIP, a Promising Biomarker That Promotes the Progression and Metastasis of Colorectal and Other Types of Cancer.Cancers · 2022Review
- Ceritinib is a novel triple negative breast cancer therapeutic agent.Molecular cancer · 2022Article
- Colorectal liver metastasis: molecular mechanism and interventional therapy.Signal transduction and targeted therapy · 2022Review
- The phosphatase of regenerating liver-3 protein (PRL-3) promotes glioma cell invasiveness by interacting with β3 -tubulin.Bioengineered · 2022Article
- PRL-3 and MMP9 Expression and Epithelial-Mesenchymal Transition Markers in Circulating Tumor Cells From Patients With Colorectal Cancer: Potential Value in Clinical Practice.Frontiers in oncology · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metastasis-associated phosphatase of regenerating liver-3 (PRL-3) has pleiotropic effects in driving cancer progression, yet the signaling mechanisms of PRL-3 are still not fully understood. Here, we provide evidence for PRL-3-induced hyperactivation of EGFR and its downstream signaling cascades in multiple human cancer cell lines. Mechanistically, PRL-3-induced activation of EGFR was attributed primarily to transcriptional downregulation of protein tyrosine phosphatase 1B (PTP1B), an inhibitory phosphatase for EGFR. Functionally, PRL-3-induced hyperactivation of EGFR correlated with increased cell growth, promigratory characteristics, and tumorigenicity. Moreover, PRL-3 induced cellular addiction to EGFR signaling, as evidenced by the pronounced reversion of these oncogenic attributes upon EGFR-specific inhibition. Of clinical significance, we verified elevated PRL-3 expression as a predictive marker for favorable therapeutic response in a heterogeneous colorectal cancer (CRC) patient cohort treated with the clinically approved anti-EGFR antibody cetuximab. The identification of PRL-3-driven EGFR hyperactivation and consequential addiction to EGFR signaling opens new avenues for inhibiting PRL-3-driven cancer progression. We propose that elevated PRL-3 expression is an important clinical predictive biomarker for favorable anti-EGFR cancer therapy.
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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.