ArticleOncogene2006
Ras-dependent carbon metabolism and transformation in mouse fibroblasts.
Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 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
65 citing papers in PubMed, 109 citations in OpenAlex.
- Recent Advances in the Development of Metal-Glycoconjugates for Medicinal Applications.Molecules (Basel, Switzerland) · 2025Review
- Glucose- and glutamine-driven de novo nucleotide synthesis facilitates WSSV replication in shrimp.Cell communication and signaling : CCS · 2025Article
- Causal relationship analysis of MRI measurements of major human internal organs and liver disease.European journal of medical research · 2025Article
- Image-Based Measures of Obesity are Associated with Alterations in Metabolic Pathways in Non-small Cell Lung Cancer.Annals of surgical oncology · 2025Article
- Imaging prediction ofThe British journal of radiology · 2023Article
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- Multifaceted roles of mitochondrial dysfunction in diseases: from powerhouses to saboteurs.Archives of pharmacal research · 2023Review
- Tumor heterogeneity: preclinical models, emerging technologies, and future applications.Frontiers in oncology · 2023Review
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- RIP140 inhibits glycolysis-dependent proliferation of breast cancer cells by regulating GLUT3 expression through transcriptional crosstalk between hypoxia induced factor and p53.Cellular and molecular life sciences : CMLS · 2022Article
- Unraveling and targeting RAS-driven metabolic signaling for therapeutic gain.Advances in cancer research · 2022Review
- Effect ofFrontiers in cell and developmental biology · 2022Article
- Iqgap3-Ras axis drives stem cell proliferation in the stomach corpus during homoeostasis and repair.Gut · 2021Article
- Identification of a targetable KRAS-mutant epithelial population in non-small cell lung cancer.Communications biology · 2021Article
- Suppression of the HBP Function Increases Pancreatic Cancer Cell Sensitivity to a Pan-RAS Inhibitor.Cells · 2021Article
- Article
- Natural Products Attenuating Biosynthesis, Processing, and Activity of Ras Oncoproteins: State of the Art and Future Perspectives.Biomolecules · 2020Review
- Reduced replication origin licensing selectively kills KRAS-mutant colorectal cancer cells via mitotic catastrophe.Cell death & disease · 2020Article
- Proteomic Analysis of Vocal Fold Fibroblasts Exposed to Cigarette Smoke Extract: Exploring the Pathophysiology of Reinke's Edema.Molecular & cellular proteomics : MCP · 2019Article
- Synthetic miR-143 Exhibited an Anti-Cancer Effect via the Downregulation of K-RAS Networks of Renal Cell Cancer Cells In Vitro and In Vivo.Molecular therapy : the journal of the American Society of Gene Therapy · 2019Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutational activation of ras genes is required for the onset and maintenance of different malignancies. Here we show, using a combination of molecular physiology, nutritional perturbations and transcriptional profiling, that full penetrance of phenotypes related to oncogenic Ras activation, including the shift of carbon metabolism towards fermentation and upregulation of key cell cycle regulators, is dependent upon glucose availability. These responses are induced by Ras activation, being specifically reverted by downregulation of the Ras pathway obtained through the expression of a dominant-negative Ras-specific guanine nucleotide exchange protein. Our data allow to link directly to ras activation the alteration in energy metabolism of cancer cells, their fragility towards glucose shortage and ensuing apoptotic death.
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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.