ArticleThe Journal of clinical investigation2015
Rare codons capacitate Kras-driven de novo tumorigenesis.
Article in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 78 citations in OpenAlex.
- RNA modifications in cancer and their detection: a review.Japanese journal of clinical oncology · 2026Review
- Maf1 cooperates with progesterone receptor to repress RNA polymerase III transcription of select tRNAs.Nucleic acids research · 2025Article
- Elucidating Ras protein as a dual therapeutic target for inflammation and cancer: a review.Discover oncology · 2025Review
- "Undruggable KRAS": druggable after all.Genes & development · 2025Review
- Dysregulation of tRNA methylation in cancer: Mechanisms and targeting therapeutic strategies.Cell death discovery · 2024Review
- Different Oncogenes and Reproductive Histories Shape the Progression of Distinct Premalignant Clones in Multistage Mouse Breast Cancer Models.The American journal of pathology · 2024Article
- Orb2 enables rare-codon-enriched mRNA expression during Drosophila neuron differentiation.Nature communications · 2024Article
- Article
- Transfer RNAs as dynamic and critical regulators of cancer progression.Nature reviews. Cancer · 2023Review
- Navigating the ERK1/2 MAPK Cascade.Biomolecules · 2023Review
- Article
- Computational Random Mutagenesis to Investigate RAS Mutant Signaling.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Article
- Functional and biological heterogeneity of KRASScience signaling · 2022Article
- Protein synthesis control in cancer: selectivity and therapeutic targeting.The EMBO journal · 2022Review
- Article
- Codon optimality in cancer.Oncogene · 2021Review
- KRAS G12C Mutations in NSCLC: From Target to Resistance.Cancers · 2021Review
- Article
- The origins and genetic interactions of KRAS mutations are allele- and tissue-specific.Nature communications · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The KRAS gene is commonly mutated in human cancers, rendering the encoded small GTPase constitutively active and oncogenic. This gene has the unusual feature of being enriched for rare codons, which limit protein expression. Here, to determine the effect of the rare codon bias of the KRAS gene on de novo tumorigenesis, we introduced synonymous mutations that converted rare codons into common codons in exon 3 of the Kras gene in mice. Compared with control animals, mice with at least 1 copy of this Kras(ex3op) allele had fewer tumors following carcinogen exposure, and this allele was mutated less often, with weaker oncogenic mutations in these tumors. This reduction in tumorigenesis was attributable to higher expression of the Kras(ex3op) allele, which induced growth arrest when oncogenic and exhibited tumor-suppressive activity when not mutated. Together, our data indicate that the inherent rare codon bias of KRAS plays an integral role in tumorigenesis.
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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.