ArticleAnnals of hematology2023
m6A methyltransferase METTL3 facilitates multiple myeloma cell growth through the m6A modification of BZW2.
Article in Annals of hematology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 14 citations in OpenAlex.
- Targeting METTL3/m6A/SOCS3 axis reprograms tumor-associated macrophage polarization to potentiate the efficacy of anti-PD-1 therapy in multiple myeloma.Cellular and molecular life sciences : CMLS · 2026Article
- m6A-methylated circFANCB Promotes Gastric Cancer Progression by Regulating Cellular Ferroptosis Through miR-454-3p/CEACAM5.Journal of biochemical and molecular toxicology · 2026Article
- Defining the RNA Modification Landscape of Multiple Myeloma Reveals METTL3-Dependent mbioRxiv : the preprint server for biology · 2026Article
- Emerging roles of RNA mInternational journal of oncology · 2026Review
- m6A methylation-modified ETV1 drives multiple myeloma progression and M2 polarization of tumor-associated macrophage through transcriptional activation of RBMS1.Journal of translational medicine · 2026Article
- FTO-Mediated m6A Demethylation of SERPINF1 Attenuates Multiple Myeloma Progression via the Wnt/β-Catenin Pathway.Journal of microbiology and biotechnology · 2026Article
- NSUN2-mediated RNA mScientific reports · 2025Article
- Mechanisms underlying hepatocellular carcinoma progression through N6-methyladenosine modifications of long non-coding RNA.World journal of gastroenterology · 2025Article
- From bone marrow mesenchymal stem cells to diseases: the crucial role of mStem cell research & therapy · 2025Review
- Research progress on N6-methyladenosine and non-coding RNA in multiple myeloma.Discover oncology · 2025Review
- N6-methyladenosine-mediated upregulation of H19 promotes resistance to bortezomib by modulating the miR-184/CARM1 axis in multiple myeloma.Clinical and experimental medicine · 2025Article
- Review
- N6-methyladenosine-induced miR-182-5p promotes multiple myeloma tumorigenesis by regulating CAMK2N1.Molecular and cellular biochemistry · 2024Article
- Novel Insights into the Links between N6-Methyladenosine and Regulated Cell Death in Musculoskeletal Diseases.Biomolecules · 2024Review
- N6-methyladenosine-modified circ_0000337 sustains bortezomib resistance in multiple myeloma by regulating DNA repair.Frontiers in cell and developmental biology · 2024Article
- The complex nature of lncRNA-mediated chromatin dynamics in multiple myeloma.Frontiers in oncology · 2023Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
N6-methyladenosine (m6A) methyltransferase-like 3 (METTL3) has been confirmed to be involved in multiple myeloma (MM) progression, and basic leucine zipper and W2 domains 2 (BZW2) is considered to be a regulator for MM development. However, whether METTL3 mediates MM progression by regulating BZW2 remains unclear. The messenger RNA (mRNA) and protein levels of METTL3 and BZW2 in MM specimens and cells were determined using quantitative real-time PCR and western blot analysis. Cell proliferation and apoptosis were assessed by cell counting kit 8 assay, 5-ethynyl-2'-deoxyuridine assay, colony formation assay, and flow cytometry. Methylated RNA immunoprecipitation-qPCR was used to detect the m6A modification level of BZW2. Xenograft tumor models were constructed to confirm the effect of METTL3 knockdown on MM tumor growth in vivo. Our results showed that BZW2 was upregulated in MM bone marrow specimens and cells. BZW2 downregulation reduced MM cell proliferation and promoted apoptosis, while its overexpression enhanced MM cell proliferation and inhibited apoptosis. METTL3 was highly expressed in MM bone marrow specimens, and its expression was positively correlated with BZW2 expression. BZW2 expression was positively regulated by METTL3. Mechanistically, METTL3 could upregulate BZW2 expression by modulating its m6A modification. Additionally, METTL3 accelerated MM cell proliferation and restrained apoptosis via increasing BZW2 expression. In vivo experiments showed that METTL3 knockdown reduced MM tumor growth by decreasing BZW2 expression. In conclusion, these data indicated that METTL3-mediated the m6A methylation of BZW2 to promote MM progression, suggesting a novel therapeutic target for MM.
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