ArticleCancer research2016
Phosphatase PTP4A3 Promotes Triple-Negative Breast Cancer Growth and Predicts Poor Patient Survival.
Article in Cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.
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Who cites it
60 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.
- A systematic review of datasets that can help elucidate relationships among gene expression, race, and immunohistochemistry-defined subtypes in breast cancer.Cancer biology & therapy · 2021Pooled it
- Review
- Integrated single-cell and spatial mapping coupled with machine learning unveils core stemness landscapes and regulatory drivers in triple-negative breast cancer.Discover oncology · 2026Article
- A Lamp2a-linked RNA secreted by ADSCs prevents ENO1-lactylation-glycolysis feedback and cell malignant behavior in triple-negative breast cancer.Cell death & disease · 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
- Ferroptosis-related gene signature-based subtype identification of triple-negative breast cancer to prioritize treatment strategies.Frontiers in oncology · 2025Article
- A multispectral 3D live organoid imaging platform to screen probes for fluorescence guided surgery.EMBO molecular medicine · 2024Article
- Article
- Protein Tyrosine Phosphatase PRL-3: A Key Player in Cancer Signaling.Biomolecules · 2024Review
- Identification of genes and pathways associated with menopausal status in breast cancer patients using two algorithms.BMC women's health · 2024Article
- Changes of Mutations and Copy-Number and Enhanced Cell Migration during Breast Tumorigenesis.Advanced biology · 2023Article
- Obesity promotes radioresistance through SERPINE1-mediated aggressiveness and DNA repair of triple-negative breast cancer.Cell death & disease · 2023Article
- Article
- PRL3 as a therapeutic target for novel cancer immunotherapy in multiple cancer types.Theranostics · 2023Review
- Knockdown of SPON2 inhibits the growth of triple-negative breast cancer.Frontiers in oncology · 2023Article
- Cisplatin or Doxorubicin Reduces Cell Viability via the PTPIVA3-JAK2-STAT3 Cascade in Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2023Article
- The phosphatase of regenerating liver-3 protein (PRL-3) promotes glioma cell invasiveness by interacting with β3 -tubulin.Bioengineered · 2022Article
- Integrative multiomics analysis identifies a metastasis-related gene signature and the potential oncogenic role of EZR in breast cancer.Oncology research · 2022Article
- Severe, but not moderate asthmatics share blood transcriptomic changes with post-traumatic stress disorder and depression.PloS one · 2022Article
- Cyclin-Dependent Kinase Inhibitors Function as Potential Immune RegulatorsFrontiers in oncology · 2022Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Triple-negative breast cancer (TNBC) has the worst prognosis of all breast cancers, and women diagnosed with TNBC currently lack targeted treatment options. To identify novel targets for TNBC, we evaluated phosphatase expression in breast tumors and characterized their contributions to in vitro and in vivo growth of TNBC. Using Affymetrix microarray analysis of 102 breast cancers, we identified 146 phosphatases that were significantly differentially expressed in TNBC compared with estrogen receptor (ER)-positive tumors. Of these, 19 phosphatases were upregulated (0.66-fold; FDR = 0.05) in TNBC compared with ER-positive breast cancers. We knocked down 17 overexpressed phosphatases in four triple-negative and four ER-positive breast cancer lines using specific siRNAs and found that depletion of six of these phosphatases significantly reduced growth and anchorage-independent growth of TNBC cells to a greater extent than ER-positive cell lines. Further analysis of the phosphatase PTP4A3 (also known as PRL-3) demonstrated its requirement for G1-S cell-cycle progression in all breast cancer cells, but PTP4A3 regulated apoptosis selectively in TNBC cells. In addition, PTP4A3 inhibition reduced the growth of TNBC tumors in vivo Moreover, in silico analysis revealed the PTP4A3 gene to be amplified in 29% of basal-like breast cancers, and high expression of PTP4A3 could serve as an independent prognostic indicator for worse overall survival. Collectively, these studies define the importance of phosphatase overexpression in TNBC and lay the foundation for the development of new targeted therapies directed against phosphatases or their respective signaling pathways for TNBC patients. Cancer Res; 76(7); 1942-53. ©2016 AACR.
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