ArticleAmerican journal of translational research2015
STAT3 signaling pathway is involved in decitabine induced biological phenotype regulation of acute myeloid leukemia cells.
Article in American journal of translational research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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The trial behind it
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- cGAS/STING-mediated upregulation of NKG2D ligands in LSCs contributes to enhanced sensitivity to NK cells.Frontiers in oncology · 2026Article
- STAT3 in acute myeloid leukemia facilitates natural killer cell-mediated surveillance.Frontiers in immunology · 2024Article
- Review
- The Multifaceted Role of STAT3 in NK-Cell Tumor Surveillance.Frontiers in immunology · 2022Review
- The Emerging Role of Suppressors of Cytokine Signaling (SOCS) in the Development and Progression of Leukemia.Cancers · 2021Review
- DNA methyltransferases in hematological malignancies.Journal of genetics and genomics = Yi chuan xue bao · 2020Review
- Interleukin-22 modulates cisplatin sensitivity of osteosarcoma cells by regulating the STAT3 signaling pathway.Experimental and therapeutic medicine · 2020Article
- Rapamycin downregulates NKG2D ligands in acute myeloid leukemia cells via an activation of the STAT3 pathway: a potential mechanism for rapamycin-induced immune escape in leukemia.Translational cancer research · 2019Article
- Serendipity: decitabine monotherapy induced complete molecular response in a 77-year-old patient with acute promyelocytic leukemia.Haematologica · 2019Article
- Decitabine enhances cytotoxic effect of T cells with an anti-CD19 chimeric antigen receptor in treatment of lymphoma.OncoTargets and therapy · 2019Article
- Article
- Natural Killer Cell Response to Chemotherapy-Stressed Cancer Cells: Role in Tumor Immunosurveillance.Frontiers in immunology · 2017Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThis study aimed to investigate the role of signal transduction and transcriptional activator STAT3 and relevant signaling pathway in the DAC regulated biological phenotype of AML cells.
methodsThe effect of DAC at different concentrations on the proliferation of HL-60 cells was determined. After DAC treatment for 48 h, the killing capability of NK cells against HL-60 cells and the protein expressions of STAT3, JAK1, JAK2, SOCS-1 and SOCS-3 were evaluated.
resultsDAC markedly inhibited the proliferation of HL-60 cells. After the treatment of 48 hr with 0.2, 0.5 and 1.0 mol/L DAC, the HL-60 viability was reduced by 25±13%, 39±8% and 50±7% (P<0.01), respectively, and the early apoptosis rate was increased to 24.77±7.5%, 27.1±4.48% and 30.53±3.93%, respectively (control: 3.11±0.12%, P<0.01). DAC up-regulated the expression of MICA/B, ULBP-1 and ULBP-3 in HL-60 cells, and increased the killing activity of NK cells to HL-60 cells. DAC significantly induced the apoptosis of HL-60 cells and up-regulated the expression of NKG2D ligands in a dose dependent manner. Western blot assay showed the protein expression of STAT3, JAK, JAK2, phosphorylated STAT3, phosphorylated JAK1 and phosphorylated JAK2 decreased, while that of SOCS-1 and SOCS-3 increased in HL-60 cells after DAC treatment.
conclusionIn HL-60 cells, DAC can markedly inhibit their proliferation and up-regulate the expression of NKG2D ligands, and DAC also increase the cytotoxicity of NK cells to HL-60 cells, which may be related to the STAT3 related signaling pathway.
Indexed as
Identifiers
26692933PMC4656766W2306049040What 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.