ArticleClinical cancer research : an official journal of the American Association for Cancer Research2008
Loss of protein inhibitors of activated STAT-3 expression in glioblastoma multiforme tumors: implications for STAT-3 activation and gene expression.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.
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Who cites it
101 citing papers in PubMed, 185 citations in OpenAlex.
- The JAK/STAT pathway: a pivotal therapeutic target in disease and advances in natural product modulation.Molecular diversity · 2026Review
- Three Thiol-Reactive Reagents drive Synergistic Lethality in Glioblastoma cells.Research square · 2026Article
- Probing the Depths of Molecular Complexity: STAT3 as a Key Architect in Colorectal Cancer Pathogenesis.Current gene therapy · 2025Review
- STAT3 Protein-Protein Interaction Analysis Finds P300 as a Regulator of STAT3 and Histone 3 Lysine 27 Acetylation in Pericytes.Biomedicines · 2024Article
- Pyrimidine compounds BY4003 and BY4008 inhibit glioblastoma cells growth via modulating JAK3/STAT3 signaling pathway.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Article
- Review
- Interplay of miRNAs and lncRNAs in STAT3 signaling pathway in colorectal cancer progression.Cancer cell international · 2024Review
- PIAS family gene expression: implications for prognosis, immunomodulation, and chemotherapy response.American journal of translational research · 2024Article
- PIAS family in cancer: from basic mechanisms to clinical applications.Frontiers in oncology · 2024Review
- Resveratrol Enhances Temozolomide Efficacy in Glioblastoma Cells through Downregulated MGMT and Negative Regulators-Related STAT3 Inactivation.International journal of molecular sciences · 2023Article
- Bufalin suppresses esophageal squamous cell carcinoma progression by activating the PIAS3/STAT3 signaling pathway.Journal of thoracic disease · 2023Article
- Comprehensive pan-cancer analysis of STAT3 as a prognostic and immunological biomarker.Scientific reports · 2023Article
- Roles of STAT3 in the pathogenesis and treatment of glioblastoma.Frontiers in cell and developmental biology · 2023Review
- Colony‑stimulating factor CSF2 mediates the phenotypic plasticity of small‑cell lung cancer by regulating the p‑STAT3/MYC pathway.Oncology reports · 2022Article
- G-CSF/GM-CSF-induced hematopoietic dysregulation in the progression of solid tumors.FEBS open bio · 2022Review
- Transcription Factors with Targeting Potential in Gliomas.International journal of molecular sciences · 2022Review
- The Role of SUMO E3 Ligases in Signaling Pathway of Cancer Cells.International journal of molecular sciences · 2022Review
- Blood-Brain Barrier Alterations and Edema Formation in Different Brain Mass Lesions.Frontiers in cellular neuroscience · 2022Review
- SOCS proteins and their roles in the development of glioblastoma.Oncology letters · 2022Review
- IL-17A Mediates Demyelination by Activating A1 AstrocytesFrontiers in immunology · 2022Article
41 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
purposeSTATs activate transcription in response to numerous cytokines, controlling proliferation, gene expression, and apoptosis. Aberrant activation of STAT proteins, particularly STAT-3, is implicated in the pathogenesis of many cancers, including GBM, by promoting cell cycle progression, stimulating angiogenesis, and impairing tumor immune surveillance. Little is known about the endogenous STAT inhibitors, the PIAS proteins, in human malignancies. The objective of this study was to examine the expression of STAT-3 and its negative regulator, PIAS3, in human tissue samples from control and GBM brains. EXPERIMENTAL
designControl and GBM human tissues were analyzed by immunoblotting and immunohistochemistry to determine the activation status of STAT-3 and expression of the PIAS3 protein. The functional consequence of PIAS3 inhibition by small interfering RNA or PIAS3 overexpression in GBM cells was determined by examining cell proliferation, STAT-3 transcriptional activity, and STAT-3 target gene expression. This was accomplished using [(3)H]TdR incorporation, STAT-3 dominant-negative constructs, reverse transcription-PCR, and immunoblotting. RESULTS AND
conclusionsSTAT-3 activation, as assessed by tyrosine and serine phosphorylation, was elevated in GBM tissue compared with control tissue. Interestingly, we observed expression of PIAS3 in control tissue, whereas PIAS3 protein expression in GBM tissue was greatly reduced. Inhibition of PIAS3 resulted in enhanced glioblastoma cellular proliferation. Conversely, PIAS3 overexpression inhibited STAT-3 transcriptional activity, expression of STAT-3-regulated genes, and cell proliferation. We propose that the loss of PIAS3 in GBM contributes to enhanced STAT-3 transcriptional activity and subsequent cell proliferation.
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