ArticleCancer science2014
Downregulation of miR-217 correlates with resistance of Ph(+) leukemia cells to ABL tyrosine kinase inhibitors.
Article in Cancer science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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Who cites it
34 citing papers in PubMed, 60 citations in OpenAlex.
- Potential of extracellular vesicle-derived microRNAs as a platform for biomarker discovery in acute lymphoblastic leukemia.PloS one · 2026Article
- MicroRNAs as Sensitizers of Tyrosine Kinase Inhibitor Resistance in Cancer: Small Molecule Partnerships.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Benchmarking miRNA reference genes in B-cell precursor acute lymphoblastic leukemia.Scientific reports · 2024Article
- Construction of Lentiviral Vector for miR-217 Overexpression and Knockdown and Its Effect on CML.Molecular biotechnology · 2023Article
- DNMT3A governs tyrosine kinase inhibitors responses through IAPs and in a cell senescence-dependent manner in non-small cell lung cancer.American journal of cancer research · 2023Article
- miR-217-5p suppresses epithelial-mesenchymal transition and the NF-κB signaling pathway in breast cancer via targeting of metadherin.Oncology letters · 2022Article
- Investigation the Cytotoxicity of 5-AZA on Acute Lymphoblastic Leukemia Cell Line In Vitro and Characterization the Underlying Molecular Mechanisms of Cell Death and Motility.Asian Pacific journal of cancer prevention : APJCP · 2021Article
- Dysregulation of miRNA in Leukemia: Exploiting miRNA Expression Profiles as Biomarkers.International journal of molecular sciences · 2021Review
- Improving Gemcitabine Sensitivity in Pancreatic Cancer Cells by Restoring miRNA-217 Levels.Biomolecules · 2021Article
- Targeting Abnormal Hematopoietic Stem Cells in Chronic Myeloid Leukemia and Philadelphia Chromosome-Negative Classical Myeloproliferative Neoplasms.International journal of molecular sciences · 2021Review
- Association of Genetic Variants in miR-217 Gene with Risk of Coronary Artery Disease: A Case-Control Study.Pharmacogenomics and personalized medicine · 2021Article
- MicroRNAs: Diverse Mechanisms of Action and Their Potential Applications as Cancer Epi-Therapeutics.Biomolecules · 2020Review
- MicroRNAs as potential therapeutics to enhance chemosensitivity in advanced prostate cancer.Scientific reports · 2018Article
- Concise Review: Chronic Myeloid Leukemia: Stem Cell Niche and Response to Pharmacologic Treatment.Stem cells translational medicine · 2018Review
- Regulation of actin-binding protein ANLN by antitumorOncotarget · 2017Article
- MicroRNAs as prognostic biomarker and relapse indicator in leukemia.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2017Review
- MicroRNA-9 plays a role in interleukin-10-mediated expression of E-cadherin in acute myelogenous leukemia cells.Cancer science · 2017Article
- miR-217 inhibits triple-negative breast cancer cell growth, migration, and invasion through targeting KLF5.PloS one · 2017Article
- Therapeutic Resistance in Acute Myeloid Leukemia: The Role of Non-Coding RNAs.International journal of molecular sciences · 2016Review
- Upregulation of miR-181c inhibits chemoresistance by targeting ST8SIA4 in chronic myelocytic leukemia.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study found that long-term exposure of chronic myelogenous leukemia (CML) K562 cells to BCR/ABL thyrosine kinase inhibitors (TKI) caused drug-resistance in association with an increase in levels of DNA methyltransferases (DNMT) and a decrease in levels of microRNA miR-217. These observations are clinically relevant; an increase in levels of DNMT3A in association with downregulation of miR-217 were noted in leukemia cells isolated from individuals with BCR/ABL TKI-resistant Philadelphia chromosome positive acute lymphoblastic leukemia (Ph(+) ALL) and CML. Further studies with TKI-resistant K562 cells found that forced expression of miR-217 inhibited expression of DNMT3A through a miR-217-binding site within the 3'-untranslated region of DNMT3A and sensitized these cells to growth inhibition mediated by the TKI. Of note, long-term exposure of K562 cells to dasatinib (10 nM) together with 5-Aza-2'-deoxycytidine (5-AzadC) (0.1 μM) potently inhibited proliferation of these cells in association with upregulation of miR-217 and downregulation of DNMT3A in vitro. In addition, a decrease in levels of DNMT3A and an increase in levels of miR-217 were noted in K562 tumors growing in immune-deficient mice that were treated with the combination of 5-AzadC and dasatinib. Taken together, Ph(+) leukemia cells acquire TKI resistance via downregulation of miR-217 and upregulation of DNMT3A. Inhibition of DNMT3A by forced expression of miR-217 or 5-AzadC may be useful to prevent drug resistance in individuals who receive TKI.
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Registered trials
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