ArticleCommunications biology2024
Aberrant NSUN2-mediated m5C modification of exosomal LncRNA MALAT1 induced RANKL-mediated bone destruction in multiple myeloma.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Genetic evidence reveals phosphatidylcholine as a mediator in the causal relationship between omega-3 and multiple myeloma risk.Scientific reports · 2025Pooled it
- Exosome-derived LncRNAs in bone remodeling: recent advances and future directions for bone disease therapy.Stem cell research & therapy · 2026Review
- The crosstalk network of non-coding RNAs: Emerging opportunities for the clinical application of osteoporosis.Non-coding RNA research · 2026Review
- RNA-Based Therapeutic Strategies in Multiple Myeloma: From Molecular Targets to Delivery and Clinical Translation.International journal of molecular sciences · 2026Review
- NSUN2-Mediated mInternational journal of general medicine · 2026Review
- Myeloma-derived exosomal circ_0002724 promotes osteoclastogenesis through a miR-4753-3p/IFIT1 and RANK axis in myeloma bone disease.Frontiers in oncology · 2026Article
- Long non-coding RNAs in the exosomal network: dual roles and clinical implications in cancer.Animal cells and systems · 2026Review
- Extracellular vesicles in multiple myeloma-bone marrow niche crosstalk: from cellular dialogue to clinical perspectives.Journal of translational medicine · 2025Review
- RNA m5C methylation in cancer: mechanisms and biological impact.Oncogenesis · 2025Review
- MALAT1 as a molecular driver of tumor progression, immune evasion, and resistance to therapy.Molecular cancer · 2025Review
- Regulatory role of the METTL3/MALAT1 axis in multiple myeloma progression.Journal of bone oncology · 2025Article
- NSUN2-mediated RNA mScientific reports · 2025Article
- CX3CL1 promotes M1 macrophage polarization and osteoclast differentiation via NSUN5-mediated m5C modification.Scientific reports · 2025Article
- Sending the Signal to Bone: How Tumor-Derived EVs Orchestrate Pre-Metastatic Niche Formation and Skeletal Colonization.Biomedicines · 2025Review
- m5C RNA methylation in cancer: from biological mechanism to clinical perspectives.European journal of medical research · 2025Review
- 5-Methylcytosine RNA modification and its roles in cancer and cancer chemotherapy resistance.Journal of translational medicine · 2025Review
- Mechanistic insights into bone destruction in multiple myeloma: Cellular and molecular perspectives.Journal of bone oncology · 2025Review
- Roles and mechanisms of NSUN2-mediated RNA mFrontiers in immunology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
The impact of exosome-mediated crosstalk between multiple myeloma (MM) cells and osteoclasts (OCs) on bone lesions remains to be investigated. Here, we identified NSUN2 and YBX1-mediated m5C modifications upregulated LncRNA MALAT1 expression in MM cells, which could be transported to OCs via exosomes and promote bone lesions. Methodologically, RNA-seq was carried out to detect the cargoes of exosomes. TRAP staining and WB were used to evaluate osteoclastogenesis in vitro. Micro-CT and bone histomorphometric analyses were performed to identify bone destruction in vivo. RNA pull-down, RIP, MeRIP, and luciferase reporter assays were used to test the interactions between molecules. The clinical features of MALAT1, NSUN2 and YBX1 were verified through public datasets and clinicopathological data analyses. Mechanistically, MALAT1 was the highest expressed lncRNA in U266 exosomes and could be transported to RAW264.7 cells. MALAT1 could enhance the differentiation of RAW264.7 cells into OCs by stimulating RANKL expression and its downstream AKT and MAPKs signaling pathways via a ceRNA mechanism. Additionally, MALAT1 could be modified by NSUN2, an m5C methyltransferase, which in turn stabilized MALAT1 through the "reader" YBX1. Clinical studies indicated a notable positive correlation between MALAT1, NSUN2, YBX1 levels and bone destruction features, as well as with RANKL expression.
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Registered trials
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.