ArticlebioRxiv : the preprint server for biology2025
RBM15-MKL1 fusion protein promotes leukemia via m6A methylation and WNT pathway activation.
Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
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Who cites it
1 citing paper in PubMed.
- Role of N6-methyladenosine methyltransferase component RBM15 in cancer progression and its therapeutic potential.Discover oncology · 2025Review
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Authors and funding
14 authors.
Funding
Abstract
Acute megakaryoblastic leukemia driven by the RBM15-MKL1 fusion protein (RM-AMKL) is the only known recurrent mutation involving the N6-methyladenosine (m6A) writer complex. Dysregulation of m6A modification affects RNA fate and is linked to oncogenesis. Inhibition of m6A deposition via inhibition of the METTL3 writer protein has anti-tumour activity, but the mechanism underlying its efficacy and cancer specificity remains unclear. We treated murine RM-AMKL cells with a novel METTL3 inhibitor, STM3675, and showed apoptosis Key Points: RM retains functional abilities of RBM15 and additionally interacts with Wnt-related transcripts to increase expression of Fzd proteins.The METTL3 writer complex and WNT signalling pathways are essential for RM-driven leukemia.
Identifiers
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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.