ArticleMolecular oncology2017
Sorafenib analogue SC-60 induces apoptosis through the SHP-1/STAT3 pathway and enhances docetaxel cytotoxicity in triple-negative breast cancer cells.
Article in Molecular oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- STAT3 as a potential therapeutic target in triple negative breast cancer: a systematic review.Journal of experimental & clinical cancer research : CR · 2019Pooled it
- Shp1 phosphatase regulates CXCR2 protein stability and IL8-mediated invasiveness in breast cancer.Cell death & disease · 2026Article
- Development and optimisation of Polyelectrolyte Complex Nanoparticles Loaded with Sorafenib by Central Composite Design (CCD): In Vitro and In Vivo Studies for the Treatment of Triple Negative Breast Cancer.Pharmaceutical research · 2025Article
- Research progress of SHP-1 agonists as a strategy for tumor therapy.Molecular diversity · 2025Review
- Pan-cancer analysis of the prognostic and immunological roles of SHP-1/ptpn6.Scientific reports · 2024Article
- Network-based approach elucidates critical genes in BRCA subtypes and chemotherapy response in triple negative breast cancer.iScience · 2024Article
- Consideration of SHP-1 as a Molecular Target for Tumor Therapy.International journal of molecular sciences · 2023Review
- Development and validation of an inflammatory response-related signature in triple negative breast cancer for predicting prognosis and immunotherapy.Frontiers in oncology · 2023Article
- Article
- Interfering B cell receptor signaling via SHP-1/p-Lyn axis shows therapeutic potential in diffuse large B-cell lymphoma.Molecular medicine (Cambridge, Mass.) · 2022Article
- Targeting regulated cell death (RCD) with small-molecule compounds in triple-negative breast cancer: a revisited perspective from molecular mechanisms to targeted therapies.Journal of hematology & oncology · 2022Review
- Article
- Prognostic Signature Development on the Basis of Macrophage Phagocytosis-Mediated Oxidative Phosphorylation in Bladder Cancer.Oxidative medicine and cellular longevity · 2022Article
- Distinct Somatic Alteration Features Identified by Gene Panel Sequencing in Korean Triple-Negative Breast Cancer with High Ki67 Expression.Diagnostics (Basel, Switzerland) · 2021Article
- Shp1 in Solid Cancers and Their Therapy.Frontiers in oncology · 2020Review
- The Analysis of PTPN6 for Bladder Cancer: An Exploratory Study Based on TCGA.Disease markers · 2020Article
- Targeting SET to restore PP2A activity disrupts an oncogenic CIP2A-feedforward loop and impairs triple negative breast cancer progression.EBioMedicine · 2019Article
- Lycorine exerts antitumor activity against osteosarcoma cells in vitro and in vivo xenograft model through the JAK2/STAT3 pathway.OncoTargets and therapy · 2019Article
- Quinalizarin Induces Apoptosis through Reactive Oxygen Species (ROS)-Mediated Mitogen-Activated Protein Kinase (MAPK) and Signal Transducer and Activator of Transcription 3 (STAT3) Signaling Pathways in Colorectal Cancer Cells.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- TIPE3 protein promotes breast cancer metastasis through activating AKT and NF-κB signaling pathways.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recurrent triple-negative breast cancer (TNBC) needs new therapeutic targets. Src homology region 2 domain-containing phosphatase-1 (SHP-1) can act as a tumor suppressor by dephosphorylating oncogenic kinases. One major target of SHP-1 is STAT3, which is highly activated in TNBC. In this study, we tested a sorafenib analogue SC-60, which lacks angiokinase inhibition activity, but acts as a SHP-1 agonist, in TNBC cells. SC-60 inhibited proliferation and induced apoptosis by dephosphorylating STAT3 in both a dose- and time-dependent manner in TNBC cells (MDA-MB-231, MDA-MB-468, and HCC1937). By contrast, ectopic expression of STAT3 rescued the anticancer effect induced by SC-60. SC-60 also increased the SHP-1 activity, but this effect was inhibited when the N-SH2 domain (DN1) was deleted or with SHP-1 point mutation (D61A), implying that SHP-1 is the major target of SC-60 in TNBC. The use of SC-60 in combination with docetaxel synergized the anticancer effect induced by SC-60 through the SHP-1/STAT3 pathway in TNBC cells. Importantly, SC-60 also displayed a significant antitumor effect in an MDA-MB-468 xenograft model by modulating the SHP-1/STAT3 axis, indicating the anticancer potential of SC-60 in TNBC treatment. Targeting SHP-1/p-STAT3 and the potential combination of SHP-1 agonist with chemotherapeutic docetaxel is a feasible therapeutic strategy for TNBC.
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