ArticleJournal of cellular and molecular medicine2019
Establishment and molecular characterization of decitabine-resistant K562 cells.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- ID1 in hematopoiesis and hematologic disorders: novel potentials of a classic differentiation regulator.Cellular & molecular biology letters · 2025Review
- Cellular immunity analysis by a modular acoustofluidic platform: CIAMAP.Science advances · 2023Article
- Abnormal regulation of miR-29b-ID1 signaling is involved in the process of decitabine resistance in leukemia cells.Cell cycle (Georgetown, Tex.) · 2023Article
- Gene Expression Profiles Identify Biomarkers of Resistance to Decitabine in Myelodysplastic Syndromes.Cells · 2021Article
- Abnormal expression and methylation of PRR34-AS1 are associated with adverse outcomes in acute myeloid leukemia.Cancer medicine · 2021Article
- Establishment and molecular characterization of decitabine-resistant K562 cells.Journal of cellular and molecular medicine · 2019Article
- Down-regulation of miR-29c is a prognostic biomarker in acute myeloid leukemia and can reduce the sensitivity of leukemic cells to decitabine.Cancer cell international · 2019Article
- The KH domain facilitates the substrate specificity and unwinding processivity of DDX43 helicase.The Journal of biological chemistryArticle
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The clinical activity of decitabine (5-aza-2-deoxycytidine, DAC), a hypomethylating agent, has been demonstrated in acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) patients. However, secondary resistance to this agent often occurs during treatment and leads to treatment failure. It is important to clarify the mechanisms underlying the resistance for improving the efficacy. In this study, by gradually increasing concentration after a continuous induction of DAC, we established the DAC-resistant K562 cell line (K562/DAC) from its parental cell line K562. The proliferation and survival rate of K562/DAC was significantly increased, whereas the apoptosis rate was remarkably decreased than that of K562 after DAC treatment. In K562/DAC, a total of 108 genes were upregulated and 118 genes were downregulated by RNA-Seq. In addition, we also observed aberrant expression of DDX43/H19/miR-186 axis (increased DDX43/H19 and decreased miR-186) in K562/DAC cells. Ectopic expression of DDX43 in parental K562 cells rendered cells resistant to the DAC. Taken together, we successfully established DAC-resistant K562 cell line which can serve as a good model for investigating DAC resistance mechanisms, and DDX43/H19/miR-186 may be involved in DAC resistance in K562.
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