ArticleJournal of translational medicine2022
Tumor-suppressive MEG3 induces microRNA-493-5p expression to reduce arabinocytosine chemoresistance of acute myeloid leukemia cells by downregulating the METTL3/MYC axis.
Article in Journal of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 36 citations in OpenAlex.
- Investigation of the Expression Levels of miR-383, miR-381, and miR-141 miRNAs as Diagnostic Biomarkers in Acute Myeloid Leukemia.International journal of laboratory hematology · 2026Article
- Exploring the Clinical Landscape of Long Non-coding RNAs in Cancer Diagnosis and Therapy.Biochemical genetics · 2026Review
- Long Non-Coding RNA Expression in B-Cell Precursor Acute Lymphoblastic Leukemia: Analysis of LINC-PINT, MEG3, BALR6, and ZEB1-AS1.Life (Basel, Switzerland) · 2026Article
- Unleashing lncRNA THOR: roles in cancer progression and clinical outlook.Molecular genetics and genomics : MGG · 2026Review
- Reflecting on 30 years of miRNA biology in malignant hematology: current challenges and future directions.Blood advances · 2025Review
- Recent advances in drug delivery and treatment strategies for acute myeloid leukemia.International journal of pharmaceutics · 2025Review
- Identification of disulfidptosis-related long non-coding RNA signature to predict the prognosis, immunotherapy, and chemotherapy options in acute myeloid leukemia.Translational cancer research · 2025Article
- METTL3: a multifunctional regulator in diseases.Molecular and cellular biochemistry · 2025Review
- METTL3/YTDHF1 Stabilizes CSRP1 mRNA to Regulate Glycolysis and Promote Acute Myeloid Leukemia Progression.Cell biochemistry and biophysics · 2025Article
- M6A-modified BFSP1 induces aerobic glycolysis to promote liver cancer growth and metastasis through upregulating tropomodulin 4.Molecular biomedicine · 2025Article
- Identification of HOXA9 methylation as an epigenetic biomarker predicting prognosis and guiding treatment choice in acute myeloid leukemia.BMC cancer · 2025Article
- The epitranscriptome meets non-coding RNA: m6A-mediated regulation in oncogenesis and therapy.Frontiers in cell and developmental biology · 2025Review
- The YTHDC1-m6A-MEG3 Regulatory Axis in Radiation-Induced Liver Injury: Deciphering Early-Stage Epitranscriptomic Alterations and Molecular Dynamics.Journal of inflammation research · 2025Article
- Methyltransferase-like 3-mediated RNA NFrontiers in immunology · 2025Review
- Recent Advances in the Mutual Regulation of m6A Modification and Non-Coding RNAs in Atherosclerosis.International journal of general medicine · 2025Review
- Epitranscriptomic RNA mAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- Unraveling the role of long non-coding RNAs in therapeutic resistance in acute myeloid leukemia: New prospects & challenges.Non-coding RNA research · 2024Review
- Intracellular Fusobacterium nucleatum infection increases METTL3-mediated m6A methylation to promote the metastasis of esophageal squamous cell carcinoma.Journal of advanced research · 2024Article
- Overview of the interplay between m6A methylation modification and non-coding RNA and their impact on tumor cells.Translational cancer research · 2024Review
- Small molecule inhibitors targeting mJournal of hematology & oncology · 2024Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChemoresistance serves as a huge obstacle for acute myeloid leukemia (AML) patients. To counteract the chemoresistance in AML cells, we discussed the role of maternally expressed gene 3 (MEG3) in arabinocytosine (AraC) chemoresistance in AML cells.
methodsMEG3, microRNA (miR)-493-5p, methyltransferase-like 3 (METTL3) and MYC expression in AML cells was determined and then their interactions were also analyzed. Then, the viability and apoptosis of AML cells were determined through loss- and gain- function assay. The level of m6A modification in AML cells was examined. AML mouse models were also established to validate the potential roles of MEG3.
resultsMEG3 and miR-493-5p were downregulated in AML cells, and they were lower in resistant cells than in parental cells. MEG3 led to elevated expression of miR-493-5p which targeted METTL3. METTL3 increased expression of MYC by promoting its m6A levels. Overexpression of MEG3 and miR-493-5p or knockdown of METTL3 inhibited HL-60 and Molm13 cell proliferation and promoted their apoptosis. Overexpressed MEG3 induced heightened sensitivity of AML cells to AraC. However, the suppression of miR-493-5p reversed the effects of overexpressed MEG3 on AML cells.
conclusionsCollectively, MEG3 could upregulate miR-493-5p expression and suppress the METTL3/MYC axis through MYC m6A methylation, by which MEG3 promoted the chemosensitivity of AML cells.
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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.