ArticleThe Journal of biological chemistry2024
Endogenous oncogenic KRAS expression increases cell proliferation and motility in near-diploid hTERT RPE-1 cells.
Article in The Journal of biological chemistry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Constitutively active RAS prolongs Cdc42 signalling, while MAPK signalling is attenuated during fission yeast mating.PLoS genetics · 2026Article
- Generation of Human Haematopoietic Model Cell Lines Revealed Distinct Replication Stress Tolerance Between Two OncogenicBiomolecules · 2026Article
- Activating KRAS mutations mark premalignant cystic structures in congenital pulmonary airway malformations.Respiratory research · 2026Article
- Breast cancer cells utilize T3 to trigger proliferation through cellular CaCell communication and signaling : CCS · 2024Article
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Authors and funding
7 authors.
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Abstract
About 18% of all human cancers carry a mutation in the KRAS gene making it among the most sought-after anticancer targets. However, mutant KRas protein has proved remarkably undruggable. The recent approval of the first generation of RAS inhibitors therefore marks a seminal milestone in the history of cancer research. It also raises the predictable challenges of limited drug efficacies and acquired resistance. Hence, new approaches that improve our understanding of the tumorigenic mechanisms of oncogenic RAS within more physiological settings continue to be essential. Here, we have used the near-diploid hTERT RPE-1 cells to generate isogenic cell lines in which one of the endogenous KRAS alleles carries an oncogenic KRAS mutation at glycine 12. Cells with a KRAS
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