ArticleThe Journal of biological chemistry2013
Identification of mutant K-Ras-dependent phenotypes using a panel of isogenic cell lines.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed.
- Differential effects of KRAS G-domain and hypervariable region mutants on cancer phenotypes.Scientific reports · 2025Article
- SEC-MX: an approach to systematically study the interplay between protein assembly states and phosphorylation.Nature communications · 2025Article
- Whole-cell energy modeling reveals quantitative changes of predicted energy flows in RAS mutant cancer cell lines.iScience · 2023Article
- Inhibition of RAS-driven signaling and tumorigenesis with a pan-RAS monobody targeting the Switch I/II pocket.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Suppression of mutant Kirsten-RAS (KRASOncogene · 2022Article
- Identification of the nucleotide-free state as a therapeutic vulnerability for inhibition of selected oncogenic RAS mutants.Cell reports · 2022Article
- Identification and validation of four photodynamic therapy related genes inhibiting MAPK and inducing cell cycle alteration in squamous cell carcinoma.Frontiers in oncology · 2022Article
- Loss of the wild-type KRAS allele promotes pancreatic cancer progression through functional activation of YAP1.Oncogene · 2021Article
- Metabonomics study of the effects of single copy mutant KRAS in the presence or absence of WT allele using human HCT116 isogenic cell lines.Metabolomics : Official journal of the Metabolomic Society · 2021Article
- EndoBind detects endogenous protein-protein interactions in real time.Communications biology · 2021Article
- KRAS phosphorylation regulates cell polarization and tumorigenic properties in colorectal cancer.Oncogene · 2021Article
- Common and mutation specific phenotypes of KRAS and BRAF mutations in colorectal cancer cells revealed by integrative -omics analysis.Journal of experimental & clinical cancer research : CR · 2021Article
- Metabolic characterization of colorectal cancer cells harbouring different KRAS mutations in codon 12, 13, 61 and 146 using human SW48 isogenic cell lines.Metabolomics : Official journal of the Metabolomic Society · 2020Article
- The proprotein convertase furin is a pro-oncogenic driver in KRAS and BRAF driven colorectal cancer.Oncogene · 2020Article
- Therapeutic targeting of RAS: New hope for drugging the "undruggable".Biochimica et biophysica acta. Molecular cell research · 2020Review
- KRAS G13D sensitivity to neurofibromin-mediated GTP hydrolysis.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Targeting plasma membrane phosphatidylserine content to inhibit oncogenic KRAS function.Life science alliance · 2019Article
- An Inhibitor of the Pleckstrin Homology Domain of CNK1 Selectively Blocks the Growth of Mutant KRAS Cells and Tumors.Cancer research · 2019Article
- KRASScience signaling · 2019Article
- Isoform-specific Ras signaling is growth factor dependent.Molecular biology of the cell · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
To assess the consequences of endogenous mutant K-Ras, we analyzed the signaling and biological properties of a small panel of isogenic cell lines. These include the cancer cell lines DLD1, HCT116, and Hec1A, in which either the WT or mutant K-ras allele has been disrupted, and SW48 colorectal cancer cells and human mammary epithelial cells in which a single copy of mutant K-ras was introduced at its endogenous genomic locus. We find that single copy mutant K-Ras causes surprisingly modest activation of downstream signaling to ERK and Akt. In contrast, a negative feedback signaling loop to EGFR and N-Ras occurs in some, but not all, of these cell lines. Mutant K-Ras also had relatively minor effects on cell proliferation and cell migration but more dramatic effects on cell transformation as assessed by growth in soft agar. Surprisingly, knock-out of the wild type K-ras allele consistently increased growth in soft agar, suggesting tumor-suppressive properties of this gene under these conditions. Finally, we examined the effects of single copy mutant K-Ras on global gene expression. Although transcriptional programs triggered by mutant K-Ras were generally quite distinct in the different cell lines, there was a small number of genes that were consistently overexpressed, and these could be used to monitor K-Ras inhibition in a panel of human tumor cell lines. We conclude that there are conserved components of mutant K-Ras signaling and phenotypes but that many depend on cell context and environmental cues.
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.