ReviewCell communication and signaling : CCS2026
Nonsense-mediated mRNA decay: friend or foe in cancer biology?
Review in Cell communication and signaling : CCS, 2026. 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
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
1 citing paper in PubMed.
- mRNA processing in cancer immunotherapy: emerging targets, resistance mechanisms, and therapeutic opportunities.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Nonsense-mediated mRNA decay (NMD) is a highly conserved RNA surveillance mechanism in eukaryotic cells. It plays a key role in safeguarding the accuracy of gene expression by eliminating mRNAs with premature termination codons (PTCs) in the cellular transcriptome. Furthermore, NMD fine-tunes gene expression by regulating the stability of numerous transcripts that harbor NMD-inducing features other than PTC. Emerging evidence has established NMD factors as key regulators in diverse biological processes, including embryonic development, tissue homeostasis, and tumor biology. This review focuses on the dual roles of NMD in tumorigenesis, cancer therapy, and their underlying mechanisms. NMD can promote tumorigenesis and progression by degrading PTC-containing mRNA variants arising from mutated tumor suppressor genes or by suppressing neoantigen expression. Conversely, NMD can exert tumor-suppressive effects by eliminating aberrant transcripts of certain oncogenes. The function of NMD in tumor dynamics is highly dependent on multiple factors, including the tumor's genetic background, the expression and mutation status of NMD factors, alternative splicing coupled to NMD (AS-NMD), and the tumor microenvironment. Moreover, we summarize cancer therapeutic strategies targeting NMD, especially NMD inhibitors (e.g., NMDI-1, NMDI-14, and 5-azacytidine). The synergistic potentials of combining NMD inhibition with nonsense mutation readthrough therapy, immune checkpoint blockade, and chemotherapy in cancer therapy are summarized. Finally, we provide perspectives on future research directions, emphasizing that a deeper understanding of the context-specific mechanisms of NMD in different tumors is crucial for developing precise anti-cancer therapies.
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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.