ArticleOncogene2002
Inhibition of constitutively active Stat3 suppresses proliferation and induces apoptosis in glioblastoma multiforme cells.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 198 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
198 citing papers in PubMed, 373 citations in OpenAlex.
- Trial
- The JAK/STAT pathway: a pivotal therapeutic target in disease and advances in natural product modulation.Molecular diversity · 2026Review
- Temozolomide and ruxolitinib combination modulates miRNA-associated regulatory networks in glioblastoma stem cells.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- First-in-child phase I trial of p-STAT3 inhibitor WP1066 in pediatric brain tumor patients.JCI insight · 2026Article
- Calanquinone A suppresses glioma progression via STAT3-mediated regulation of c-Myc and MMP9.Discover oncology · 2025Article
- Tumor heterogeneity and resistance in glioblastoma: the role of stem cells.Apoptosis : an international journal on programmed cell death · 2025Review
- Interplay Between Key Molecular Signaling Pathways and Immune Players Following Brain Irradiation.Mediators of inflammation · 2025Review
- Interleukin 6 and cancer resistance in glioblastoma multiforme.Neurosurgical review · 2024Review
- Interleukin 4 and cancer resistance in glioblastoma multiforme.Neurosurgical review · 2024Review
- From bench to bedside: the past, present and future of IL-21 immunotherapy.Medical oncology (Northwood, London, England) · 2024Review
- Mechanistic insights and the clinical prospects of targeted therapies for glioblastoma: a comprehensive review.Experimental hematology & oncology · 2024Review
- 'Slicing' glioblastoma drivers with the Swiss cheese model.Trends in cancer · 2024Review
- Novel sights on therapeutic, prognostic, and diagnostics aspects of non-coding RNAs in glioblastoma multiforme.Metabolic brain disease · 2023Review
- KLF13 Regulates the Activity of the GH-Induced JAK/STAT Signaling by Targeting Genes Involved in the Pathway.International journal of molecular sciences · 2023Article
- Cancer and Alzheimer's Inverse Correlation: an Immunogenetic Analysis.Molecular neurobiology · 2023Review
- Effect of Photobiomodulation on Protein Kinase Cδ, Cytochrome C, and Mitochondria in U87 MG Cells.Cells · 2023Article
- Differential roles of type I interferon signaling in tumor versus host cells in experimental glioma models.Translational oncology · 2023Article
- Development and validation of an inflammatory response-related prognostic model and immune infiltration analysis in glioblastoma.Annals of translational medicine · 2023Article
- Sphingosine kinase 1 promotes growth of glioblastoma by increasing inflammation mediated by the NF-Acta pharmaceutica Sinica. B · 2022Article
- Potential Therapeutic Effects of Thiazolidinedione on Malignant Glioma.International journal of molecular sciences · 2022Article
138 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Glioblastoma multiforme (GBM), the most common and malignant central nervous system tumor in humans, is highly proliferative and resistant to apoptosis. Stat3, a latent transcription factor being activated by aberrant cytokine or growth factor signaling, acts as a suppressor of apoptosis in a number of cancer cells. Here we report that GBM tumors and cell lines contain high levels of constitutively activated Stat3 when compared with normal human astrocytes, white matter, and normal tissue adjacent to tumor. The persistent activation of Stat3 is in part, attributable to an autocrine action of interleukin-6 in the GBM cell line U251. Janus kinase inhibitor AG490 inhibits Stat3 activation with a concomitant reduction in steady-state levels of Bcl-X(L), Bcl-2 and Mcl-1 proteins and induces apoptosis in U251 cells as revealed by Poly (ADP-ribose) polymerase cleavage and Annexin-V staining. Expression of a dominant negative mutant Stat3 protein or treatment with AG490 markedly reduces the proliferation of U251 cells by inhibiting the constitutive activation of Stat3. These results provide evidence that constitutive activation of Stat3 contributes to the pathogenesis of glioblastoma by promoting both proliferation and survival of GBM cells. Therefore, targeting Stat3 signaling may provide a potential therapeutic intervention for GBM.
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.