ArticleBiomolecules & therapeutics2017
LncRNA MEG3 Regulates Imatinib Resistance in Chronic Myeloid Leukemia via Suppressing MicroRNA-21.
Article in Biomolecules & therapeutics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 78 citations in OpenAlex.
- Long non-coding RNAs and therapeutic resistance in multiple myeloma: from molecular insights to clinical applications.Clinical and experimental medicine · 2026Review
- The multiplex crosstalk between non-coding RNAs, programmed cell death and related mechanisms: a dynamic duo in hematological malignancies.Cancer cell international · 2025Review
- Combined replacement of lnc-MEG3 and miR-155 elicit tumor suppression in multiple myeloma.Epigenomics · 2025Article
- Impact of non-coding RNAs on resistance to imatinib in chronic myelogenous leukemia.Leukemia research reports · 2025Review
- Non-coding RNAs: Emerging contributors to chemoresistance in chronic myeloid leukemia.Leukemia research reports · 2025Review
- microRNA 21 and long non-coding RNAs interplays underlie cancer pathophysiology: A narrative review.Non-coding RNA research · 2024Review
- LncRNATranslational cancer research · 2024Article
- Non-coding RNAs in leukemia drug resistance: new perspectives on molecular mechanisms and signaling pathways.Annals of hematology · 2024Review
- Article
- The Role of Long Noncoding RNAs in Progression of Leukemia: Based on Chromosomal Location.MicroRNA (Shariqah, United Arab Emirates) · 2024Review
- Long non-coding RNAs regulate treatment outcome in leukemia: What have we learnt recently?Cancer medicine · 2023Review
- The Biological Roles and Molecular Mechanisms of Long Non-Coding RNA MEG3 in the Hallmarks of Cancer.Cancers · 2022Review
- Diagnostic and Therapeutic Implications of Long Non-Coding RNAs in Leukemia.Life (Basel, Switzerland) · 2022Review
- Non-Coding RNAs Are Implicit in Chronic Myeloid Leukemia Therapy Resistance.International journal of molecular sciences · 2022Review
- Long Noncoding RNAs That Function in Nutrition: Lnc-ing Nutritional Cues to Metabolic Pathways.Annual review of nutrition · 2022Review
- Long non-coding RNA MEG3 regulates the progress of osteoarthritis by regulating the miR-34a/Klotho axis.Annals of translational medicine · 2022Article
- A novel imatinib-upregulated long noncoding RNA plays a critical role in inhibition of tumor growth induced by Abl oncogenes.Molecular cancer · 2022Article
- A review of current evidence about lncRNA MEG3: A tumor suppressor in multiple cancers.Frontiers in cell and developmental biology · 2022Review
- Non-coding RNAs: are they the protagonist or antagonist in the regulation of leukemia?American journal of translational research · 2022Review
- Reducing LncRNA-5657 expression inhibits the brain inflammatory reaction in septic rats.Neural regeneration research · 2021Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Imatinib resistance has become a major clinical problem for chronic myeloid leukemia. The aim of the present study was to investigate the involvement of MEG3, a lncRNA, in imatinib resistance and demonstrate its underlying mechanisms. RNAs were extracted from CML patients' peripheral blood cells and human leukemic K562 cells, and the expression of MEG3 was measured by RT-qPCR. Cell proliferation and cell apoptosis were evaluated. Western blotting was used to measure the protein expression of several multidrug resistant transporters. Luciferase reporter assay was performed to determine the binding between MEG3 and miR-21. Our results showed that MEG3 was significantly decreased in imatinib-resistant CML patients and imatinib-resistant K562 cells. Overexpression of MEG3 in imatinib-resistant K562 cells markedly decreased cell proliferation, increased cell apoptosis, reversed imatinib resistance, and reduced the expression of MRP1, MDR1, and ABCG2. Interestingly, MEG3 binds to miR-21. MEG3 and miR-21 were negatively correlated in CML patients. In addition, miR-21 mimics reversed the phenotype of MEG3-overexpression in imatinib-resistant K562 cells. Taken together, MEG3 is involved in imatinib resistance in CML and possibly contributes to imatinib resistance through regulating miR-21, and subsequent cell proliferation, apoptosis and expression of multidrug resistant transporters.
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Registered trials
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