Evidence map›Paper›PMID 42260649›Full record

ReviewCell communication and signaling : CCS2026

Nonsense-mediated mRNA decay: friend or foe in cancer biology?

Yuhui Wang, Chenghai He, Chengyan Chen, Xin Ma, Xiyao Gao, Guodong Li, Tangliang Li

Abstract readReview
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Yuhui Wang *Zhejiang Key Laboratory of Medical Epigenetics, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou, 311121, China.
Chenghai He *Department of Gastroenterology, The Affiliated Hospital of Hangzhou Normal University, Hangzhou, 311121, China.
Chengyan Chen *Zhejiang Key Laboratory of Medical Epigenetics, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou, 311121, China.
Xin MaCollege of Animal Science and Technology, Qingdao Agricultural University, Qingdao, 266109, China.
Xiyao GaoZhejiang Key Laboratory of Medical Epigenetics, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou, 311121, China.
Guodong LiDepartment of Gastroenterology, The Affiliated Hospital of Hangzhou Normal University, Hangzhou, 311121, China. hzseliguodong@sina.com.
Tangliang LiZhejiang Key Laboratory of Medical Epigenetics, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou, 311121, China. li.tangliang@hznu.edu.cn.

Funding

Natural Science Foundation of Shandong Province ZR2023MC013Natural Science Foundation of Shandong Province ZR2024QC193Postdoctoral Innovation Project of Shandong Province SDCX-ZG-202303003Scientific Research Fund of Zhejiang Provincial Education Department Y202558079
6 · The paper itself

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.

Indexed as

NeoplasmsNonsense Mediated mRNA DecayAnimalsCodon, NonsenseHumansRNA, MessengerCodon, NonsenseRNA, MessengerCancer therapymRNA decayNeoantigenNMD inhibitionPremature termination codon

Identifiers

PMID42260649
PMCPMC13471619

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.