ArticleThe American journal of pathology2010
PTP1B suppresses prolactin activation of Stat5 in breast cancer cells.
Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 52 citations in OpenAlex.
- Design, synthesis, molecular docking and anticancer activity evaluation of methyl salicylate based thiazoles as PTP1B inhibitors.Scientific reports · 2025Article
- Reduction of phosphorylated signal transducer and activator of transcription-5 expression in feline mammary carcinoma.The Journal of veterinary medical science · 2024Article
- Protein Tyrosine Phosphatase 1B (PTP1B): A Comprehensive Review of Its Role in Pathogenesis of Human Diseases.International journal of molecular sciences · 2024Review
- STAT family of transcription factors in breast cancer: Pathogenesis and therapeutic opportunities and challenges.Seminars in cancer biology · 2022Review
- Tyrosine phosphatases regulate resistance to ALK inhibitors in ALK+ anaplastic large cell lymphoma.Blood · 2022Article
- Prolactin receptor gene transcriptional control, regulatory modalities relevant to breast cancer resistance and invasiveness.Frontiers in endocrinology · 2022Review
- Review
- The Attenuated Secretion of Hyaluronan by UVA-Exposed Human Fibroblasts Is Associated with Up- and Downregulation of HYBID and HAS2 Expression via Activated and Inactivated Signaling of the p38/ATF2 and JAK2/STAT3 Cascades.International journal of molecular sciences · 2021Article
- Neuronal protein-tyrosine phosphatase 1B hinders sensory-motor functional recovery and causes affective disorders in two different focal ischemic stroke models.Neural regeneration research · 2021Article
- RAB6 GTPase regulates mammary secretory function by controlling the activation of STAT5.Development (Cambridge, England) · 2020Article
- Involvement of STAT5 in Oncogenesis.Biomedicines · 2020Review
- Drosophila Jak/STAT Signaling: Regulation and Relevance in Human Cancer and Metastasis.International journal of molecular sciences · 2018Review
- Prolactin and oleic acid synergistically stimulate β-cell proliferation and growth in rat islets.Islets · 2017Article
- β-Arrestin 1's Interaction with TC45 Attenuates Stat signaling by dephosphorylating Stat to inhibit antimicrobial peptide expression.Scientific reports · 2016Article
- Validation of tumor protein marker quantification by two independent automated immunofluorescence image analysis platforms.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2016Article
- The Protein Tyrosine Kinase Inhibitor Tyrphostin 23 Strongly Accelerates Glycolytic Lactate Production in Cultured Primary Astrocytes.Neurochemical research · 2016Article
- Downregulated Expression of PTPN9 Contributes to Human Hepatocellular Carcinoma Growth and Progression.Pathology oncology research : POR · 2016Article
- Scribble is required for pregnancy-induced alveologenesis in the adult mammary gland.Journal of cell science · 2016Article
- Article
- Src family kinases interfere with dimerization of STAT5A through a phosphotyrosine-SH2 domain interaction.Cell communication and signaling : CCS · 2015Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Basal levels of nuclear localized, tyrosine phosphorylated Stat5 are present in healthy human breast epithelia. In contrast, Stat5 phosphorylation is frequently lost during breast cancer progression, a finding that correlates with loss of histological differentiation and poor patient prognosis. Identifying the mechanisms underlying loss of Stat5 phosphorylation could provide novel targets for breast cancer therapy. Pervanadate, a general tyrosine phosphatase inhibitor, revealed marked phosphatase regulation of Stat5 activity in breast cancer cells. Lentiviral-mediated shRNA allowed specific examination of the regulatory role of five tyrosine phosphatases (PTP1B, TC-PTP, SHP1, SHP2, and VHR), previously implicated in Stat5 regulation in various systems. Enhanced and sustained prolactin-induced Stat5 tyrosine phosphorylation was observed in T47D and MCF7 breast cancer cells selectively in response to PTP1B depletion. Conversely, PTP1B overexpression suppressed prolactin-induced Stat5 tyrosine phosphorylation. Furthermore, PTP1B knockdown increased Stat5 reporter gene activity. Mechanistically, PTP1B suppression of Stat5 phosphorylation was mediated, at least in part, through inhibitory dephosphorylation of the Stat5 tyrosine kinase, Jak2. PTP1B knockdown enhanced sensitivity of T47D cells to prolactin phosphorylation of Stat5 by reducing the EC(50) from 7.2 nmol/L to 2.5 nmol/L. Immunohistochemical analyses of two independent clinical breast cancer materials revealed significant negative correlations between levels of active Stat5 and PTP1B, but not TC-PTP. Collectively, our data implicate PTP1B as an important negative regulator of Stat5 phosphorylation in invasive breast cancer.
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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.