ArticleNature genetics2021
The amino acid transporter SLC7A5 is required for efficient growth of KRAS-mutant colorectal cancer.
Article in Nature genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 177 papers, 3 of them syntheses that pooled it.
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Who cites it
177 citing papers in PubMed, 3 syntheses or guidelines pooled it, 324 citations in OpenAlex.
- A systematic review of omics discovery studies to identify pertinent metabolic pathways for locally advanced rectal cancer in response to neoadjuvant chemoradiotherapy.Metabolomics : Official journal of the Metabolomic Society · 2025Pooled it
- Current hotspots and trends in cancer metabolic reprogramming: a scientometric analysis.Frontiers in immunology · 2024Pooled it
- Machine learning-based meta-analysis of colorectal cancer and inflammatory bowel disease.PloS one · 2023Pooled it
- Metabolic reprogramming in colorectal cancer: Mechanisms and therapeutic insights.Genes & diseases · 2027Review
- Branched-chain amino acids and gut microbiota: coregulation and impact on neurological function via the gut-brain axis.Gut microbes · 2026Review
- Metabolites and cancer metastasis.Oncogene · 2026Review
- Glutamine metabolism in health and disease.Signal transduction and targeted therapy · 2026Review
- Changes in the transcriptome and synthetic lethal dependencies followingProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Collagen I promotes cancer cell survival via amino acid import and mTORC1/S6 activation.PLoS biology · 2026Article
- Targeting colorectal cancer and T‑cell metabolism for the treatment of colorectal cancer (Review).Oncology reports · 2026Review
- SLC7A5 promotes colorectal cancer liver metastasis by reprogramming tryptophan metabolism through the Kyn/XANA‒AhR axis and reshaping the immune microenvironment.Clinical and translational medicine · 2026Article
- Bioengineered systems to exploit tumor microenvironment metabolism.Trends in cancer · 2026Review
- PCBP1 orchestrates amino acid metabolism burst during the naïve-to-primed pluripotency transition.Stem cell reports · 2026Article
- Article
- Integrative proteomic characterization of human lung adenocarcinoma with KRAS G12 mutations reveals molecular pathogenesis.Journal of advanced research · 2026Article
- CALB2 Expression Is Associated with Tumor Progression and Prognosis in Colorectal Adenocarcinoma.Genes · 2026Article
- Targeting glutamine metabolism to modulate macrophage functions in the tumor microenvironment.Discover oncology · 2026Review
- 18F-FDG-PET/CT-negative gastric cancer employs glutamine-based gluconeogenesis and fatty acid oxidation to support tumor growth.Cell death & disease · 2026Article
- Solute Carrier transporters in tumor metabolism and immune modulation: implications for therapy.Journal of translational medicine · 2026Review
- Metabolic reprogramming in cancer: dysregulation of glucose, lipid, and amino acid pathways and therapeutic opportunities.Molecular biomedicine · 2026Review
117 more citing papers are in PubMed but not listed here.
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43 authors at 12 institutions in 4 countries.
Funding
Abstract
Oncogenic KRAS mutations and inactivation of the APC tumor suppressor co-occur in colorectal cancer (CRC). Despite efforts to target mutant KRAS directly, most therapeutic approaches focus on downstream pathways, albeit with limited efficacy. Moreover, mutant KRAS alters the basal metabolism of cancer cells, increasing glutamine utilization to support proliferation. We show that concomitant mutation of Apc and Kras in the mouse intestinal epithelium profoundly rewires metabolism, increasing glutamine consumption. Furthermore, SLC7A5, a glutamine antiporter, is critical for colorectal tumorigenesis in models of both early- and late-stage metastatic disease. Mechanistically, SLC7A5 maintains intracellular amino acid levels following KRAS activation through transcriptional and metabolic reprogramming. This supports the increased demand for bulk protein synthesis that underpins the enhanced proliferation of KRAS-mutant cells. Moreover, targeting protein synthesis, via inhibition of the mTORC1 regulator, together with Slc7a5 deletion abrogates the growth of established Kras-mutant tumors. Together, these data suggest SLC7A5 as an attractive target for therapy-resistant KRAS-mutant CRC.
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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.