ReviewTrends in molecular medicine2022
Dysfunctional tRNA reprogramming and codon-biased translation in cancer.
Review in Trends in molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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.
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Who cites it
44 citing papers in PubMed, 61 citations in OpenAlex.
- The role of RNA modifications in cancer translational control.RNA biology · 2026Review
- RNA N4-acetylcytidine modification in health and cancer: molecular mechanisms, cellular plasticity, and therapeutic opportunities.Biomarker research · 2026Review
- Pyridoxal-phosphate-dependent biosynthesis of aminovaleramide by AvaS in tRNA.Nature chemical biology · 2026Article
- Mechanistic Insights Into the Oxidative Reactivity of 2-Selenouridine in tRNA.Chemistry (Weinheim an der Bergstrasse, Germany) · 2026Article
- URMylation Signaling Pathway in Cancer: Molecular Mechanisms and Therapeutic Opportunities.Current issues in molecular biology · 2026Review
- N7-Methylguanosine Modification in Colorectal Cancer: Molecular Insights and Clinical Implications.International journal of molecular sciences · 2026Review
- G/C-ending and synonymous codon bias define functional translational programs that shape human tissue and cancer proteomes.NAR genomics and bioinformatics · 2026Article
- Host mature tRNAome as a decoding switch regulates antiviral and proviral responses.Nature communications · 2026Article
- Probing the epitranscriptome and RNA damage with nanopore direct RNA sequencing.RNA (New York, N.Y.) · 2026Review
- tRNA modification genes are associated with genomic instability, proliferative programs, and poor prognosis in breast cancer.Breast cancer (Tokyo, Japan) · 2026Article
- Synonymous codon usage defines functional gene families.BMC biology · 2026Article
- ADAM-tRNA-seq: an optimized approach for demultiplexing and enhanced hierarchal mapping in direct tRNA sequencing.Nucleic acids research · 2026Article
- A context-dependent METTL1-m7G-SLC7A11 axis links metabolic stress to epithelial fate in ulcerative colitis.International journal of biological sciences · 2026Article
- Transfer RNA expression, modification, and derived small RNAs in cancer biology and clinical potential.Frontiers in immunology · 2026Review
- PUS1 Drives Renal Cancer Progression by Preventing Formation of Endogenous Double-stranded RNAs.International journal of biological sciences · 2026Article
- Translation elongation: measurements and applications.RNA biology · 2025Review
- ALKBH1 Drives Tumorigenesis and Drug Resistance via tRNA-decoding Reprogramming and Codon-biased Translation.Cancer discovery · 2025Article
- The tRNA Editing Complex ADAT2/3 Promotes Cancer Cell Growth and Codon-biased mRNA Translation.Journal of molecular biology · 2025Article
- Toward standardized epitranscriptome analytics: an inter-laboratory comparison of mass spectrometric detection and quantification of modified ribonucleosides in human RNA.Nucleic acids research · 2025Article
- TRMT6-mediated tRNA mNature cancer · 2025Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Many cancers hijack translation to increase the synthesis of tumor-driving proteins, the messenger mRNAs of which have specific codon usage patterns. Termed 'codon-biased translation' and originally identified in stress response regulation, this mechanism is supported by diverse studies demonstrating how the 50 RNA modifications of the epitranscriptome, specific tRNAs, and codon-biased mRNAs are used by oncogenic programs to promote proliferation and chemoresistance. The epitranscriptome writers METTL1-WDR4, Elongator complex protein (ELP)1-6, CTU1-2, and ALKBH8-TRM112 illustrate the principal mechanism of codon-biased translation, with gene amplifications, increased RNA modifications, and enhanced tRNA stability promoting cancer proliferation. Furthermore, systems-level analyses of 34 tRNA writers and 493 tRNA genes highlight the theme of tRNA epitranscriptome dysregulation in many cancers and identify candidate tRNA writers, tRNA modifications, and tRNA molecules as drivers of pathological codon-biased translation.
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What OpenQuestion holds
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.