ReviewPharmacology & therapeutics2018
Targeting phosphatases of regenerating liver (PRLs) in cancer.
Review in Pharmacology & therapeutics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 52 citations in OpenAlex.
- Article
- PTP4A2 promotes leukemogenesis through inhibiting the p53 tumor suppressor signaling pathway in leukemia-initiating cells.Blood advances · 2026Article
- 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
- Targeting of PTP4A3 overexpression sensitises HGSOC cells towards chemotherapeutic drugs.Molecular oncology · 2025Article
- Comprehensive molecular characteristics of hepatocellular carcinoma based on multi-omics analysis.BMC cancer · 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
- In silico identification of putative druggable pockets in PRL3, a significant oncology target.Biochemistry and biophysics reports · 2024Article
- Targeting PRL phosphatases in hematological malignancies.Expert opinion on therapeutic targets · 2024Review
- Targeting Moonlighting Enzymes in Cancer.Molecules (Basel, Switzerland) · 2024Review
- PRKAA2, MTOR, and TFEB in the regulation of lysosomal damage response and autophagy.Journal of molecular medicine (Berlin, Germany) · 2024Review
- Dietary Linoleic Acid: An Omega-6 Fatty Acid Essential for Liver Regeneration in Buffalo Rats.Comparative medicine · 2023Article
- 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
- HSC70 mediated autophagic degradation of oxidized PRL2 is responsible for osteoclastogenesis and inflammatory bone destruction.Cell death and differentiation · 2023Article
- Phosphatase-independent role of phosphatase of regenerating liver in cancer progression.Cancer science · 2023Review
- PRL3 as a therapeutic target for novel cancer immunotherapy in multiple cancer types.Theranostics · 2023Review
- Article
- The Tyrosine Phosphatase PRL Regulates Attachment of Toxoplasma gondii to Host Cells and Is Essential for Virulence.mSphere · 2022Article
- Anticancer Profile of Rhodanines: Structure-Activity Relationship (SAR) and Molecular Targets-A Review.Molecules (Basel, Switzerland) · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The phosphatase of regenerating liver (PRL) family, also known as protein tyrosine phosphatase 4A (PTP4A), are dual-specificity phosphatases with largely unknown cellular functions. However, accumulating evidence indicates that PRLs are oncogenic across a broad variety of human cancers. PRLs are highly expressed in advanced tumors and metastases compared to early stage cancers or matched healthy tissue, and high expression of PRLs often correlates with poor patient prognosis. Consequentially, PRLs have been considered potential therapeutic targets in cancer. Persistent efforts have been made to define their role and mechanism in cancer progression and to create specific PRL inhibitors for basic research and drug development. However, targeting PRLs with small molecules remains challenging due to the highly conserved active site of protein tyrosine phosphatases and a high degree of sequence similarity between the PRL protein families. Here, we review the current PRL inhibitors, including the strategies used for their identification, their biological efficacy, potency, and selectivity, with a special focus on how PRL structure can inform future efforts to develop specific PRL inhibitors.
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What OpenQuestion holds
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.