ArticleScientific reports2015
PRL-3 activates mTORC1 in Cancer Progression.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Phosphatases of regenerating liver downregulate PTEN to promote tumorigenesis.Biochemical Society transactions · 2026Review
- Targeting of PTP4A3 overexpression sensitises HGSOC cells towards chemotherapeutic drugs.Molecular oncology · 2025Article
- Unveiling the Role of Mechanistic Target of Rapamycin Kinase (MTOR) Signaling in Cancer Progression and the Emergence of MTOR Inhibitors as Therapeutic Strategies.ACS pharmacology & translational science · 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
- The Helix-Loop-Helix motif of human EIF3A regulates translation of proliferative cellular mRNAs.PloS one · 2023Article
- PRL3 as a therapeutic target for novel cancer immunotherapy in multiple cancer types.Theranostics · 2023Review
- PRL3 induces polypoid giant cancer cells eliminated by PRL3-zumab to reduce tumor relapse.Communications biology · 2021Article
- Revealing dynamic regulations and the related key proteins of myeloma-initiating cells by integrating experimental data into a systems biological model.Bioinformatics (Oxford, England) · 2021Article
- Increased expression of GATA zinc finger domain containing 1 through gene amplification promotes liver cancer by directly inducing phosphatase of regenerating liver 3.Hepatology (Baltimore, Md.) · 2018Article
- A loss-of-function genetic screening reveals synergistic targeting of AKT/mTOR and WTN/β-catenin pathways for treatment of AML with high PRL-3 phosphatase.Journal of hematology & oncology · 2018Article
- Article
- Control of leucine-dependent mTORC1 pathway through chemical intervention of leucyl-tRNA synthetase and RagD interaction.Nature communications · 2017Article
- PRL-3 promotes telomere deprotection and chromosomal instability.Nucleic acids research · 2017Article
- Downregulation of microRNA-100/microRNA-125b is associated with lymph node metastasis in early colorectal cancer with submucosal invasion.Cancer science · 2017Article
- Article
- Antibody Array Revealed PRL-3 Affects Protein Phosphorylation and Cytokine Secretion.PloS one · 2017Article
- PRL-3 promotes the peritoneal metastasis of gastric cancer through the PI3K/Akt signaling pathway by regulating PTEN.Oncology reports · 2016Article
- Inhibition of PRL-2·CNNM3 Protein Complex Formation Decreases Breast Cancer Proliferation and Tumor Growth.The Journal of biological chemistry · 2016Article
- Biomarkers Discovery for Colorectal Cancer: A Review on Tumor Endothelial Markers as Perspective Candidates.Disease markers · 2016Review
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PRL-3, a metastasis-associated phosphatase, is known to exert its oncogenic functions through activation of PI3K/Akt, which is a key regulator of the rapamycin-sensitive mTOR complex 1 (mTORC1), but a coherent link between PRL-3 and activation of mTOR has not yet been formally demonstrated. We report a positive correlation between PRL-3 expression and mTOR phospho-activation in clinical tumour samples and mouse models of cancer and demonstrate that PRL-3 increased downstream signalling to the mTOR substrates, p70S6K and 4E-BP1, by increasing PI3K/Akt-mediated activation of Rheb-GTP via TSC2 suppression. We also show that PRL-3 increases mTOR translocation to lysosomes via increased mTOR binding affinity to Rag GTPases in an Akt-independent manner, demonstrating a previously undescribed mechanism of action for PRL-3. PRL-3 also enhanced matrix metalloproteinase-2 secretion and cellular invasiveness via activation of mTOR, attributes which were sensitive to rapamycin treatment. The downstream effects of PRL-3 were maintained even under conditions of environmental stress, suggesting that PRL-3 provides a strategic survival advantage to tumour cells via its effects on mTOR.
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