ArticleProceedings of the National Academy of Sciences of the United States of America2020
Mutation bias within oncogene families is related to proliferation-specific codon usage.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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.
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
18 citing papers in PubMed, 29 citations in OpenAlex.
- Synonymous mutations in essential genes infrequently produce fitness effects in human cell lines.Nucleic acids research · 2026Article
- Transfer RNA expression, modification, and derived small RNAs in cancer biology and clinical potential.Frontiers in immunology · 2026Review
- ALKBH1 Drives Tumorigenesis and Drug Resistance via tRNA-decoding Reprogramming and Codon-biased Translation.Cancer discovery · 2025Article
- Viral codon usage and the virus-host interactions.Frontiers in microbiology · 2025Review
- Translation efficiency driven by CNOT3 subunit of the CCR4-NOT complex promotes leukemogenesis.Nature communications · 2024Article
- Incorporating mutational heterogeneity to identify genes that are enriched for synonymous mutations in cancer.BMC bioinformatics · 2023Article
- Navigating the ERK1/2 MAPK Cascade.Biomolecules · 2023Review
- Cancers make their own luck: theories of cancer origins.Nature reviews. Cancer · 2023Review
- Pan-cancer atlas of somatic core and linker histone mutations.NPJ genomic medicine · 2023Article
- Article
- Using CADD tools to inhibit the overexpressed genes FAP, FN1, and MMP1 by repurposing ginsenoside C and Rg1 as a treatment for oral cancer.Frontiers in molecular biosciences · 2023Article
- KRAS-related long noncoding RNAs in human cancers.Cancer gene therapy · 2022Review
- Protein synthesis control in cancer: selectivity and therapeutic targeting.The EMBO journal · 2022Review
- Pan-cancer analyses of synonymous mutations based on tissue-specific codon optimality.Computational and structural biotechnology journal · 2022Article
- Codon Usage Bias: An Endless Tale.Journal of molecular evolution · 2021Review
- Codon optimality in cancer.Oncogene · 2021Review
- Distinct signatures of codon and codon pair usage in 32 primary tumor types in the novel database CancerCoCoPUTs for cancer-specific codon usage.Genome medicine · 2021Article
- Translational efficiency across healthy and tumor tissues is proliferation-related.Molecular systems biology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is well known that in cancer gene families some members are more frequently mutated in tumor samples than their family counterparts. A paradigmatic case of this phenomenon is KRAS from the RAS family. Different explanations have been proposed ranging from differential interaction with other proteins to preferential expression or localization. Interestingly, it has been described that despite the high amino acid identity between RAS family members, KRAS employs an intriguing differential codon usage. Here, we found that this phenomenon is not exclusive to the RAS family. Indeed, in the RAS family and other oncogene families with two or three members, the most prevalently mutated gene in tumor samples employs a differential codon usage that is characteristic of genes involved in proliferation. Prompted by these observations, we chose the RAS family to experimentally demonstrate that the translation efficiency of oncogenes that are preferentially mutated in tumor samples is increased in proliferative cells compared to quiescent cells. These results were further validated by assessing the translation efficiency of KRAS in cell lines that differ in their tRNA expression profile. These differences are related to the cell division rate of the studied cells and thus suggest an important role in context-specific oncogene expression regulation. Altogether, our study demonstrates that dynamic translation programs contribute to shaping the expression profiles of oncogenes. Therefore, we propose this codon bias as a regulatory layer to control cell context-specific expression and explain the differential prevalence of mutations in certain members of oncogene families.
Indexed as
Identifiers
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.