ArticleJournal of immunology research2017
Decitabine-Induced Changes in Human Myelodysplastic Syndrome Cell Line SKM-1 Are Mediated by FOXO3A Activation.
Article in Journal of immunology research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Decitabine induces cell differentiation and growth inhibition accompanied by upregulation of microRNA-143 and MS4A3 in the myelodysplastic syndromes-derived leukemic cell line MDS-L.Oncology letters · 2026Article
- Survival predictors in Vietnamese elderly AML patients treated with decitabine: Real-world evidence from a low- and middle-income country.Leukemia research reports · 2026Article
- Restoration of Autophagy and Apoptosis in Myelodysplastic Syndromes: The Effect of Azacitidine in Disease Pathogenesis.Current issues in molecular biology · 2025Article
- Decitabine promotes the differentiation of poorly differentiated gastric cancer cells and enhances the sensitivity of NK cell cytotoxicity via TNF-α.Scientific reports · 2025Article
- U2AF1 mutation promotes tumorigenicity through facilitating autophagy flux mediated by FOXO3a activation in myelodysplastic syndromes.Cell death & disease · 2021Article
- Synergistic inhibitory effects of low-dose decitabine in combination with bortezomib in the AML cell line Kasumi-1.Experimental and therapeutic medicine · 2021Article
- Ascorbate Inhibits Proliferation and Promotes Myeloid Differentiation inFrontiers in oncology · 2021Article
- Autophagy Gene Panel-Based Prognostic Model in Myelodysplastic Syndrome.Frontiers in oncology · 2020Article
- Decitabine Induces Change of Biological Traits in Myelodysplastic Syndromes via FOXO1 Activation.Frontiers in genetics · 2020Article
- The Emerging Role of Sperm-Associated Antigen 6 Gene in the Microtubule Function of Cells and Cancer.Molecular therapy oncolytics · 2019Review
- Review
- Downregulation of microRNA‑21 expression inhibits proliferation, and induces G1 arrest and apoptosis via the PTEN/AKT pathway in SKM‑1 cells.Molecular medicine reports · 2018Article
- Under-Evaluated or Unassessed Pathogenic Pathways in Autoimmune Hepatitis and Implications for Future Management.Digestive diseases and sciences · 2018Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The epigenetic silencing of tumor suppressor genes in myelodysplastic syndromes (MDS) can potentially confer a growth advantage to individual cellular clones. Currently, the recommended treatment for patients with high-risk MDS is the methylation agent decitabine (DAC), a drug that can induce the reexpression of silenced tumor suppressor genes. We investigated the effects of DAC treatment on the myeloid MDS cell line SKM-1 and investigated the role of FOXO3A, a potentially tumor-suppressive transcription factor, by silencing its expression prior to DAC treatment. We found that FOXO3A exists in an inactive, hyperphosphorylated form in SKM-1 cells, but that DAC both induces FOXO3A expression and reactivates the protein by reducing its phosphorylation level. Furthermore, we show that this FOXO3A activation is responsible for the DAC-induced differentiation of SKM-1 cells into monocytes, as well as for SKM-1 cell cycle arrest, apoptosis, and autophagy. Collectively, these results suggest that FOXO3A reactivation may contribute to the therapeutic effects of DAC in MDS.
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