ArticleOncotarget2016
The phosphatase of regenerating liver-3 (PRL-3) is important for IL-6-mediated survival of myeloma cells.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 31 citations in OpenAlex.
- Targeting PTP4A3 with KVX-053 mitigates alcohol-amplified SARS-CoV-2 spike protein-induced acute lung injury.Frontiers in pharmacology · 2026Article
- 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
- Targeting PRL phosphatases in hematological malignancies.Expert opinion on therapeutic targets · 2024Review
- Protein Tyrosine Phosphatase PRL-3: A Key Player in Cancer Signaling.Biomolecules · 2024Review
- PRL3 as a therapeutic target for novel cancer immunotherapy in multiple cancer types.Theranostics · 2023Review
- Metabolic cross-talk within the bone marrow milieu: focus on multiple myeloma.Experimental hematology & oncology · 2022Review
- Highly expressed genes in multiple myeloma cells - what can they tell us about the disease?European journal of haematology · 2022Article
- Metabolic Vulnerabilities in Multiple Myeloma.Cancers · 2022Review
- Biological Hallmarks and Emerging Strategies to Target STAT3 Signaling in Multiple Myeloma.Cells · 2022Review
- Berberine as a Potential Anticancer Agent: A Comprehensive Review.Molecules (Basel, Switzerland) · 2021Review
- PRL-3 promotes a positive feedback loop between STAT1/2-induced gene expression and glycolysis in multiple myeloma.The FEBS journal · 2021Article
- PRL3 induces polypoid giant cancer cells eliminated by PRL3-zumab to reduce tumor relapse.Communications biology · 2021Article
- Phosphatase of regenerating liver-3 regulates cancer cell metabolism in multiple myeloma.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- A worm gel-based 3D model to elucidate the paracrine interaction between multiple myeloma and mesenchymal stem cells.Materials today. Bio · 2020Article
- Article
- Review
- Up-Regulation of Phosphatase in Regenerating Liver-3 (PRL-3) Contributes to Malignant Progression of Hepatocellular Carcinoma by Activating Phosphatase and Tensin Homolog Deleted on Chromosome Ten (PTEN)/Phosphoinositide 3-Kinase (PI3K)/AKT Signaling Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- 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
- PRL-3 promotes gastric cancer peritoneal metastasis via the PI3K/AKT signaling pathwayOncology letters · 2018Article
- Phosphatase of regenerating liver-3 is expressed in acute lymphoblastic leukemia and mediates leukemic cell adhesion, migration and drug resistance.Oncotarget · 2018Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple myeloma (MM) is a neoplastic proliferation of bone marrow plasma cells. PRL-3 is a phosphatase induced by interleukin (IL)-6 and other growth factors in MM cells and promotes MM-cell migration. PRL-3 has also been identified as a marker gene for a subgroup of patients with MM. In this study we found that forced expression of PRL-3 in the MM cell line INA-6 led to increased survival of cells that were depleted of IL-6. It also caused redistribution of cells in cell cycle, with an increased number of cells in G2M-phase. Furthermore, forced PRL-3 expression significantly increased phosphorylation of Signal transducer and activator of transcription (STAT) 3 both in the presence and the absence of IL-6. Knockdown of PRL-3 with shRNA reduced survival in MM cell line INA-6. A pharmacological inhibitor of PRL-3 reduced survival in the MM cell lines INA-6, ANBL-6, IH-1, OH-2 and RPMI8226. The inhibitor also reduced survival in 9 of 9 consecutive samples of purified primary myeloma cells. Treatment with the inhibitor down-regulated the anti-apoptotic protein Mcl-1 and led to activation of the intrinsic apoptotic pathway. Inhibition of PRL-3 also reduced IL-6-induced phosphorylation of STAT3. In conclusion, our study shows that PRL-3 is an important mediator of growth factor signaling in MM cells and hence possibly a good target for treatment of MM.
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