ArticleNature communications2017
Stat3 regulates centrosome clustering in cancer cells via Stathmin/PLK1.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
36 citing papers in PubMed, 49 citations in OpenAlex.
- The Trifecta of Polo-Like Kinases, Cancer, and the Immune System: Emerging Intersections and Therapeutic Insights.Molecular cancer research : MCR · 2026Review
- ALDH+ Anaplastic Thyroid Cancer Cells Show Vulnerability to a Pharmacologic Inducer of Centrosome Declustering.Cancer research communications · 2026Article
- ARID1A deficiency activates OSM-STAT3 axis in endometrial cancer, creating vulnerability to JAK/STAT3 inhibition.International journal of biological sciences · 2026Article
- CALB2 mediates tumor progression and immune escape in colorectal cancer by shaping an inhibitory immune microenvironment.Frontiers in immunology · 2026Article
- An mTOR-Stat3-Stathmin pathway controls centrosome and microtubule dynamics for oocyte polarization.Current biology : CB · 2025Article
- Polo-like kinase 4 (PLK4) as a therapeutic target in breast cancer.Carcinogenesis · 2025Review
- Article
- Tumor Microenvironment-Responsive Nanoparticles Enhance IDO1 Blockade Immunotherapy by Remodeling Metabolic Immunosuppression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Identification and validation of biomarkers related to centrosome replication in ulcerative colitis based on bulk transcriptome, single-cell RNA sequencing and experiments.Frontiers in immunology · 2025Article
- PTEN-deficient, chromosomal instability colorectal cancer is hypersensitive to STAT3 inhibition.International journal of biological sciences · 2025Article
- Discovery of a 6-Aminobenzo[ACS pharmacology & translational science · 2024Article
- The Eμ-Ret mouse is a novel model of hyperdiploid B-cell acute lymphoblastic leukemia.Leukemia · 2024Article
- Centrosome amplification-related signature correlated with immune microenvironment and treatment response predicts prognosis and improves diagnosis of hepatocellular carcinoma by integrating machine learning and single-cell analyses.Hepatology international · 2024Article
- Whole-Genome Duplication and Genome Instability in Cancer Cells: Double the Trouble.International journal of molecular sciences · 2023Review
- Centrosome Amplification Is a Potential Molecular Target in Paediatric Acute Lymphoblastic Leukemia.Cancers · 2022Article
- Centrosome Defects in Hematological Malignancies: Molecular Mechanisms and Therapeutic Insights.Blood science (Baltimore, Md.) · 2022Review
- Synergistic apoptotic effect of miR-183-5p and Polo-Like kinase 1 inhibitor NMS-P937 in breast cancer cells.Cell death and differentiation · 2022Article
- The SH2 domain and kinase activity of JAK2 target JAK2 to centrosome and regulate cell growth and centrosome amplification.PloS one · 2022Article
- Effects of the PLK4 inhibitor Centrinone on the biological behaviors of acute myeloid leukemia cell lines.Frontiers in genetics · 2022Article
- Effects of Aurora kinase A on mouse decidualization via Stat3-plk1-cdk1 pathway.Reproductive biology and endocrinology : RB&E · 2021Article
Corrections and comments
- Commented on by
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer cells frequently have amplified centrosomes that must be clustered together to form a bipolar mitotic spindle, and targeting centrosome clustering is considered a promising therapeutic strategy. A high-content chemical screen for inhibitors of centrosome clustering identified Stattic, a Stat3 inhibitor. Stat3 depletion and inhibition in cancer cell lines and in tumours in vivo caused significant inhibition of centrosome clustering and viability. Here we describe a transcription-independent mechanism for Stat3-mediated centrosome clustering that involves Stathmin, a Stat3 interactor involved in microtubule depolymerization, and the mitotic kinase PLK1. Furthermore, PLK4-driven centrosome amplified breast tumour cells are highly sensitive to Stat3 inhibitors. We have identified an unexpected role of Stat3 in the regulation of centrosome clustering, and this role of Stat3 may be critical in identifying tumours that are sensitive to Stat3 inhibitors.
Indexed as
Identifiers
What OpenQuestion holds
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.