ArticleCell2016
Mutant KRAS Enhances Tumor Cell Fitness by Upregulating Stress Granules.
Article in Cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers, 1 of them a synthesis that pooled it.
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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.
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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
134 citing papers in PubMed, 1 synthesis or guideline pooled it, 197 citations in OpenAlex.
- Unraveling the Genetic Web: H-Ras Expression and Mutation in Oral Squamous Cell Carcinoma-A Systematic Review.Head and neck pathology · 2024Pooled it
- Stress granules at the crossroads of the proteostasis network.RNA biology · 2026Review
- Article
- The Role of Long Noncoding RNAs in Modulation of Stress Granules in Cancer.Journal of cellular and molecular medicine · 2026Review
- M1C IS NECESSARY FOR DARAXONRASIB RESISTANCE OF NSCLC KRAS(G12C) MUTANT CELLS.bioRxiv : the preprint server for biology · 2026Article
- Stress granules promote DNA damage repair through the G3BP1/NAT10/ATF3 axis to facilitate nasopharyngeal carcinoma progression.Oncogene · 2026Article
- CAPRIN1-mediated sequestration of NCOA4 mRNA into stress granules drives sorafenib resistance in hepatocellular carcinoma.Oncogene · 2026Article
- Aurora-A drives sorafenib resistance by scaffolding stress granule assembly via phase separation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Review
- An Analysis of G3BP2 in Non-Small Cell Lung Cancer.Cancers · 2026Article
- Review
- Targeted stress granule regulation by engineering a non-catalytic O-GlcNAc transferase.Nature communications · 2026Article
- Amyloid-bodies in the evolution of malignancies.PloS one · 2026Article
- PARP10 is critical for stress granule initiation.Life science alliance · 2025Article
- Lactylation of HMGB1 at K177 Drives Nuclear Export of TIAR to Promote Hypoxia-Induced Stress Granule Formation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- In long-lasting cellular stress phases of melanoma cells, stress granules are dissolved by HSP70.Cellular and molecular life sciences : CMLS · 2025Article
- Stress granules promote quiescence by enhancing p21 levels and reducing phospho-Rb.RNA (New York, N.Y.) · 2025Article
- NSCLC cells sustain phase separation of cytoplasmic membrane-less organelles to protect themselves against cisplatin treatment.Acta pharmacologica Sinica · 2025Article
- Cancer Cell-Secreted miR-33a Reduces Stress Granule Formation by Targeting Polyamine Metabolism in Stroma to Promote Tumourigenesis.Journal of extracellular vesicles · 2025Article
- PABPC1 SUMOylation enhances cell survival by promoting mitophagy through stabilizing U-rich mRNAs within stress granules.Nature communications · 2025Article
74 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
There is growing evidence that stress-coping mechanisms represent tumor cell vulnerabilities that may function as therapeutically beneficial targets. Recent work has delineated an integrated stress adaptation mechanism that is characterized by the formation of cytoplasmic mRNA and protein foci, termed stress granules (SGs). Here, we demonstrate that SGs are markedly elevated in mutant KRAS cells following exposure to stress-inducing stimuli. The upregulation of SGs by mutant KRAS is dependent on the production of the signaling lipid molecule 15-deoxy-delta 12,14 prostaglandin J2 (15-d-PGJ2) and confers cytoprotection against stress stimuli and chemotherapeutic agents. The secretion of 15-d-PGJ2 by mutant KRAS cells is sufficient to enhance SG formation and stress resistance in cancer cells that are wild-type for KRAS. Our findings identify a mutant KRAS-dependent cell non-autonomous mechanism that may afford the establishment of a stress-resistant niche that encompasses different tumor subclones. These results should inform the design of strategies to eradicate tumor cell communities.
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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.