ArticleMolecular cancer therapeutics2014
Mutant ras elevates dependence on serum lipids and creates a synthetic lethality for rapamycin.
Article in Molecular cancer therapeutics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Lipidomic profiling of human serum enables detection of pancreatic cancer.Nature communications · 2022Article
- Unraveling and targeting RAS-driven metabolic signaling for therapeutic gain.Advances in cancer research · 2022Review
- Inhibiting glutamine utilization creates a synthetic lethality for suppression of ATP citrate lyase in KRas-driven cancer cells.PloS one · 2022Article
- KRAS mutation: from undruggable to druggable in cancer.Signal transduction and targeted therapy · 2021Review
- The Metabolic Landscape of RAS-Driven Cancers from biology to therapy.Nature cancer · 2021Review
- Albumin promotes the progression of fibroblasts through late GCell cycle (Georgetown, Tex.) · 2020Article
- Gold/alpha-lactalbumin nanoprobes for the imaging and treatment of breast cancer.Nature biomedical engineering · 2020Article
- Mammalian phospholipase D: Function, and therapeutics.Progress in lipid research · 2020Review
- Genome-wide Screen for Culture Adaptation and Tumorigenicity-Related Genes in Human Pluripotent Stem Cells.iScience · 2019Article
- Omega-3 fatty acids, membrane remodeling and cancer prevention.Molecular aspects of medicine · 2018Review
- Article
- Lipid sensing by mTOR complexes viaThe Journal of biological chemistry · 2017Article
- A Late G1 Lipid Checkpoint That Is Dysregulated in Clear Cell Renal Carcinoma Cells.The Journal of biological chemistry · 2017Article
- Fatty Acid Oxidation Mediated by Acyl-CoA Synthetase Long Chain 3 Is Required for Mutant KRAS Lung Tumorigenesis.Cell reports · 2016Article
- Blocking anaplerotic entry of glutamine into the TCA cycle sensitizes K-Ras mutant cancer cells to cytotoxic drugs.Oncogene · 2015Article
- Apoptotic effects of high-dose rapamycin occur in S-phase of the cell cycle.Cell cycle (Georgetown, Tex.) · 2015Article
- Inhibition of fatty acid synthase induces pro-survival Akt and ERK signaling in K-Ras-driven cancer cells.Cancer letters · 2014Article
- Phospholipase D and the maintenance of phosphatidic acid levels for regulation of mammalian target of rapamycin (mTOR).The Journal of biological chemistry · 2014Review
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Authors and funding
5 authors.
Funding
Abstract
The conversion of normal cells to cancer cells involves a shift from catabolic to anabolic metabolism involving increased glucose uptake and the diversion of glycolytic intermediates into nucleotides, amino acids, and lipids needed for cell growth. An underappreciated aspect of nutrient uptake is the utilization of serum lipids. We investigated the dependence of human cancer cells on serum lipids and report here that Ras-driven human cancer cells are uniquely dependent on serum lipids for both proliferation and survival. Removal of serum lipids also sensitizes Ras-driven cancer cells to rapamycin-indicating that the enhanced need for serum lipids creates a synthetic lethal phenotype that could be exploited therapeutically. Although depriving humans of serum lipids is not practical, suppressing uptake of lipids is possible. Suppressing macropinocytosis in Ras-driven cancer cells also created sensitivity to suppression of the mammalian/mechanistic target of rapamycin complex 1 (mTORC1). It is speculated that this property displayed by Ras-driven cancer cells represents an Achilles' heel for the large number of human cancers that are driven by activating Ras mutations.
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