ArticleOncotarget2016
MST3 promotes proliferation and tumorigenicity through the VAV2/Rac1 signal axis in breast cancer.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 39 citations in OpenAlex.
- VAV2-associated ncRNA network in the focal adhesion pathway is dysregulated in laryngeal squamous cell carcinoma.Discover oncology · 2026Article
- LncRNA OIP5-AS1 promotes immune evasion in abdominal aortic aneurysm cells by recruiting MDSCs and inhibiting CD8 + T cells through STK24 upregulation.Cytotechnology · 2025Article
- ROS-induced cytosolic release of mitochondrial PGAM5 promotes colorectal cancer progression by interacting with MST3.Nature communications · 2025Article
- Protein Kinase STK24 Promotes Tumor Immune Evasion via the AKT-PD-L1 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Review
- The mammalian Sterile 20-like kinase 4 (MST4) signaling in tumor progression: Implications for therapy.Cancer letters · 2023Review
- Molecular mechanisms involved in regulating protein activity and biological function of MST3.Cell division · 2023Review
- STK24 Promotes Progression of LUAD and Modulates the Immune Microenvironment.Mediators of inflammation · 2023Article
- Prognostic and Immune Infiltration Value of Proteasome Assembly Chaperone (PSMG) Family Genes in Lung Adenocarcinoma.International journal of medical sciences · 2023Article
- Article
- Prognostic and Genomic Analysis of Proteasome 20S Subunit Alpha (PSMA) Family Members in Breast Cancer.Diagnostics (Basel, Switzerland) · 2021Article
- Potential Prognostic Biomarkers of NIMA (Never in Mitosis, Gene A)-Related Kinase (NEK) Family Members in Breast Cancer.Journal of personalized medicine · 2021Article
- Article
- CCDC167 as a potential therapeutic target and regulator of cell cycle-related networks in breast cancer.Aging · 2021Article
- Proteomic Characterization of Cytoplasmic Lipid Droplets in Human Metastatic Breast Cancer Cells.Frontiers in oncology · 2021Article
- Review
- Discovery of a novel kinase hinge binder fragment by dynamic undocking.RSC medicinal chemistry · 2020Article
- Comprehensive Proteomic Characterization Reveals Subclass-Specific Molecular Aberrations within Triple-negative Breast Cancer.iScience · 2020Article
- Targeting Rac and Cdc42 GEFs in Metastatic Cancer.Frontiers in cell and developmental biology · 2020Review
- microRNA-222 promotes colorectal cancer cell migration and invasion by targeting MST3.FEBS open bio · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MST3 (mammalian STE20-like kinase 3) belongs to the Ste20 serine/threonine protein kinase family. The role of MST3 in tumor growth is less studied; therefore, we investigates the function of MST3 in breast cancer. Here, we demonstrate that MST3 is overexpressed in human breast tumors. Online Kaplan-Meier plotter analysis reveals that overexpression of MST3 predicts poor prognosis in breast cancer patients. Knockdown of MST3 with shRNA inhibits proliferation and anchorage-independent growth in vitro. Downregulation of MST3 in triple-negative MDA-MB-231 and MDA-MB-468 breast cancer cells decreases tumor formation in NOD/SCID mice. MST3 interacts with VAV2, but not VAV3, as demonstrated by co-immunoprecipitation and confocal microscopy. By domain mapping of MST3, we determine that the proline-rich region of MST3 (353KDIPKRP359) interacts with the SH3 domain of VAV2. Mutation of the two proline residues in this domain significantly attenuates the interaction between MST3 and VAV2. Overexpression of wild-type MST3 (WT-MST3), but not proline-rich-deleted MST3 (âP-MST3), enhances the proliferation rate and anchorage-independent growth of MDA-MB-468 cells. Overexpression of MST3 increases VAV2 phosphorylation and GTP-Rac1, whereas downregulation of MST3 or delivery of âP-MST3 results in a reduction of VAV2 and Rac1 activation. Knockdown of MST3 inhibits cyclin D1 protein expression. The Rac1 inhibitor EHop-016 attenuates cell proliferation induced by WT-MST3. Finally, Knockdown of MST3 or Rac1 inhibitor decreases cyclin D protein expression, which is important for tumor growth. These results indicate that MST3 interacts with VAV2 to activate Rac1 and promote the tumorigenicity of 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.