ArticleActa pharmacologica Sinica2021
G3BP1 promotes human breast cancer cell proliferation through coordinating with GSK-3β and stabilizing β-catenin.
Article in Acta pharmacologica Sinica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 32 citations in OpenAlex.
- The pro-obesity role of G3BP1 through altering adipogenic differentiation in mice via the PI3K/AKT pathway.Adipocyte · 2026Article
- Brucea javanica Oil Emulsion Promotes Breast Cancer Cell Autophagy and Apoptosis by Regulating PAX6 mRNA Stability Through the hsa_circ_0001589/G3BP1 Axis.Clinical and experimental pharmacology & physiology · 2026Article
- Unveiling isoleucyl-tRNA synthetase 2 as a novel driver of breast cancer via β-catenin pathway activation.Journal of cell communication and signaling · 2026Article
- Negative Pressure Promotes G3BP1-Mediated Migration of Corneal Epithelial Cells Through Activation of AKT/ERK/Paxillin Pathway.International journal of molecular sciences · 2026Article
- Quantitative Global Proteomics of Formalin-Fixed Paraffin-Embedded Tumors Identifies Dimethylated G3BP1 at Arginine 460 as a Robust Pharmacodynamic Biomarker of Methylthioadenosine Phosphorylase-Selective Protein Arginine Methyltransferase 5 Inhibition.Journal of proteome research · 2026Article
- Platelet Lysate-Enriched Human Induced Pluripotent Stem Cell-Derived Chondrocyte Sheets for Bone Defect Repair via Endochondral Ossification.Advanced healthcare materials · 2026Article
- Pharmacological modulation of stress granulesFrontiers in pharmacology · 2026Review
- G3BP1 reduction during cellular senescence promotes SVIL expression and selected senescence-associated phenotypes.Frontiers in cell and developmental biology · 2026Article
- Precise andACS central science · 2025Article
- Histone Demethylase UTX Suppresses Tumor Cell Proliferation by Regulating Stress Granules.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- SNORD88B promotes proliferation and invasion of trophoblast by regulating G3BP1 m6 A modification and alternative splicing.Cellular and molecular life sciences : CMLS · 2025Article
- Role of the Wnt signaling pathway in the complex microenvironment of breast cancer and prospects for therapeutic potential (Review).International journal of oncology · 2025Review
- Wnt signaling in cancer: from biomarkers to targeted therapies and clinical translation.Molecular cancer · 2025Review
- DCAF7 Acts as A Scaffold to Recruit USP10 for G3BP1 Deubiquitylation and Facilitates Chemoresistance and Metastasis in Nasopharyngeal Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Review
- USP21-mediated G3BP1 stabilization accelerates proliferation and metastasis of esophageal squamous cell carcinoma via activating Wnt/β-Catenin signaling.Oncogenesis · 2024Article
- G3BP1 Interact with JAK2 mRNA to Promote the Malignant Progression of Nasopharyngeal Carcinoma via Activating JAK2/STAT3 Signaling Pathway.International journal of biological sciences · 2024Article
- CIP2A interacts with AKT1 to promote the malignant biological behaviors of oral squamous cell carcinoma by upregulating the GSK‑3β/β‑catenin pathway.Experimental and therapeutic medicine · 2023Article
- Role(s) of G3BPs in Human Pathogenesis.The Journal of pharmacology and experimental therapeutics · 2023Review
- Stress granules: functions and mechanisms in cancer.Cell & bioscience · 2023Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ras-GTPase activating SH3 domain-binding protein 1 (G3BP1) is a multifunctional binding protein involved in the development of a variety of human cancers. However, the role of G3BP1 in breast cancer progression remains largely unknown. In this study, we report that G3BP1 is upregulated and correlated with poor prognosis in breast cancer. Overexpression of G3BP1 promotes breast cancer cell proliferation by stimulating β-catenin signaling, which upregulates a number of proliferation-related genes. We further show that G3BP1 improves the stability of β-catenin by inhibiting its ubiquitin-proteasome degradation rather than affecting the transcription of β-catenin. Mechanistically, elevated G3BP1 interacts with and inactivates GSK-3β to suppress β-catenin phosphorylation and degradation. Disturbing the G3BP1-GSK-3β interaction accelerates the degradation of β-catenin, impairing the proliferative capacity of breast cancer cells. Our study demonstrates that the regulatory mechanism of the G3BP1/GSK-3β/β-catenin axis may be a potential therapeutic target for 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.