ArticleLeukemia2009
STAT3 transcription factor is constitutively activated and is oncogenic in nasal-type NK/T-cell lymphoma.
Article in Leukemia, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 107 citations in OpenAlex.
- From molecular pathogenesis to novel Therapeutic approaches - a review of recent advances in the treatment of peripheral T cell Lymphomas.Biomarker research · 2026Review
- Review
- EBV-associated histological transformation of marginal zone lymphomas: two case reports and a literature review.Virchows Archiv : an international journal of pathology · 2026Article
- Butyrate-producingGut · 2025Article
- Advances in peripheral T cell lymphomas: pathogenesis, genetic landscapes and emerging therapeutic targets.Histopathology · 2025Review
- Review
- Analysis of mutation profiles in extranodal NK/T-cell lymphoma: clinical and prognostic correlations.Annals of hematology · 2024Article
- Targeting Bcl-xL is a potential therapeutic strategy for extranodal NK/T cell lymphoma.iScience · 2023Article
- Preclinical characterization of WB737, a potent and selective STAT3 inhibitor, in natural killer/T-cell lymphoma.MedComm · 2023Article
- Super-enhancer-driven TOX2 mediates oncogenesis in Natural Killer/T Cell Lymphoma.Molecular cancer · 2023Article
- Extranodal NK-/T-cell lymphoma, nasal type: what advances have been made in the last decade?Frontiers in oncology · 2023Review
- High-dose extended-field radiotherapy plus chemotherapy improved survival in extranodal NK/T-cell lymphoma in a real-life setting: results from the multicenter T-Cell Brazil Project.Scientific reports · 2022Observational
- Intravascular NK/T-Cell Lymphoma: What We Know about This Diagnostically Challenging, Aggressive Disease.Cancers · 2022Review
- Deregulated JAK3 mediates growth advantage and hemophagocytosis in extranodal nasal-type natural killer/T-cell lymphoma.Haematologica · 2022Article
- 3-Chloro-3-methyl-2,6-diarylpiperidin-4-ones as Anti-Cancer Agents: Synthesis, Biological Evaluation, Molecular Docking, and In Silico ADMET Prediction.Biomolecules · 2022Article
- Genomic profiling identifies distinct genetic subtypes in extra-nodal natural killer/T-cell lymphoma.Leukemia · 2022Article
- Essential role for STAT3/FOXM1/ATG7 signaling-dependent autophagy in resistance to Icotinib.Journal of experimental & clinical cancer research : CR · 2022Article
- Update on Molecular Diagnosis in Extranodal NK/T-Cell Lymphoma and Its Role in the Era of Personalized Medicine.Diagnostics (Basel, Switzerland) · 2022Review
- The Multifaceted Role of STAT3 in NK-Cell Tumor Surveillance.Frontiers in immunology · 2022Review
- The Role of PD-L1 Expression in Prediction and Stratification of Recurrent or Refractory Extranodal Natural Killer/T-Cell Lymphoma.Frontiers in oncology · 2022Article
Corrections and comments
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Authors and funding
14 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nasal-type natural killer (NK) cell lymphoma is an infrequent aggressive malignant disease with very poor prognosis. We aimed to explore the possible role of the transcription factor STAT3 in the pathophysiology of this malignancy, as it was involved in oncogenesis and chemoresistance. For this, we established and characterized a continuous interleukin 2-dependent NK cell line (MEC04) from a patient with a fatal nasal-type NK-cell lymphoma. Cells harbored poor cytotoxic activity against K562 cells, and spontaneously secreted interferon-gamma, interleukin-10 and vascular-endothelium growth factor in vitro. STAT3 was phosphorylated in Y705 dimerization residue in MEC04 cells and restricted to the nucleus. Y705 STAT3 phosphorylation involved JAK2, as exposure of cells to AG490 inhibitor inhibited Y705 STAT3 phosphorylation. By using recombinant transducible TAT-STAT3-beta (beta isoform), TAT-STAT3Y705F (a STAT3 protein mutated on Y705 residue, which prevents STAT3 dimerization) and peptides inhibiting specifically STAT3 dimerization, we inhibited STAT3 phosphorylation and cell growth, with cell death induction. Finally, STAT3 was phosphorylated in Y705 residue in the nuclei of lymphoma cells in eight/nine patients with nasal-type NK/T-cell lymphoma and in YT, another NK cell line. Our results suggest that STAT3 protein has a major role in the oncogenic process of nasal-type NK-cell lymphomas, and may represent a promising therapeutical target.
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