ArticleClinical and experimental medicine2025
N6-methyladenosine-mediated upregulation of H19 promotes resistance to bortezomib by modulating the miR-184/CARM1 axis in multiple myeloma.
Article in Clinical and experimental medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The dual role of miR-184 in cancer: a systematic review of context-dependent regulation.Molecular biology reports · 2025Pooled it
- 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
- 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
- Long non-coding RNAs and therapeutic resistance in multiple myeloma: from molecular insights to clinical applications.Clinical and experimental medicine · 2026Review
- Regulatory role of the METTL3/MALAT1 axis in multiple myeloma progression.Journal of bone oncology · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Malignant plasma cell proliferation characterizes multiple myeloma (MM), a hematologic disease. Bortezomib (BTZ) is a protease inhibitor that has been approved for the treatment of MM. Nevertheless, the effectiveness of BTZ is frequently impeded by drug resistance, and the mechanisms responsible for this phenomenon remain incompletely understood. A growing body of evidence indicates that N6-methyladenosine (m6A) plays crucial roles in a wide range of biological functions. However, the impact of m6A on the response of MM cells to BTZ is poorly understood. In our recent research, we discovered that METTL3 facilitated the m6A alteration of lncRNA H19, providing MM cells with resistance to BTZ. Additional examination revealed that H19 functioned as a sponge to negatively regulate the expression of miR-184 in MM cells. Furthermore, we discovered that H19 binds to miR-184, a tumor suppressor, in MM cells. In MM cells, miR184 can suppress the expression of CARM1 by targeting its 3'-UTR. In conclusion, rescue trials have validated the significance of the METTL3/H19/miR-184/CARM1 pathway in determining the susceptibility of cells to BTZ. Consequently, directing efforts toward this pathway could prove to be a powerful approach for enhancing the effectiveness of BTZ for MM therapy.
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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 Socratic graph.