ArticlePloS one
Single Synonymous Mutations in KRAS Cause Transformed Phenotypes in NIH3T3 Cells.
Article in PloS one. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 13 citations in OpenAlex.
- Differential effects of KRAS G-domain and hypervariable region mutants on cancer phenotypes.Scientific reports · 2025Article
- Evaluation of KRAS inhibitor-directed therapies for pancreatic cancer treatment.Frontiers in oncology · 2024Review
- Unraveling novel and rare mutations for alpha-amylase and key transcription factors in EMS-induced wheat mutants for amylose by TILLING.Molecular biology reports · 2022Article
- The emergence of the postgenomic gene.European journal for philosophy of science · 2022Article
- Mutation bias within oncogene families is related to proliferation-specific codon usage.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Development and characterization of an EMS-mutagenized wheat population and identification of salt-tolerant wheat lines.BMC plant biology · 2020Article
- Recognition of the polycistronic nature of human genes is critical to understanding the genotype-phenotype relationship.Genome research · 2018Review
- Evaluation of the selectivity and sensitivity of isoform- and mutation-specific RAS antibodies.Science signaling · 2017Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Synonymous mutations in the KRAS gene are clustered at G12, G13, and G60 in human cancers. We constructed 9 stable NIH3T3 cell lines expressing KRAS, each with one of these synonymous mutations. Compared to the negative control cell line expressing the wild type human KRAS gene, all the synonymous mutant lines expressed more KRAS protein, grew more rapidly and to higher densities, and were more invasive in multiple assays. Three of the cell lines showed dramatic loss of contact inhibition, were more refractile under phase contrast, and their refractility was greatly reduced by treatment with trametinib. Codon usage at these glycines is highly conserved in KRAS compared to HRAS, indicating selective pressure. These transformed phenotypes suggest that synonymous mutations found in driver genes such as KRAS may play a role in human cancers.
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.