ArticleJournal of cancer research and clinical oncology2018
Targeting of glutamine transporter ASCT2 and glutamine synthetase suppresses gastric cancer cell growth.
Article in Journal of cancer research and clinical oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 69 citations in OpenAlex.
- New Functions of Mitochondrial Dysfunction in Gastric Cancer: From Molecular Processes to Potential Treatments.International journal of molecular sciences · 2026Review
- Gastric Cancer: Pathobiology and Therapeutics.MedComm · 2026Review
- CD90 Promotes Gastric Cancer Progression by Regulating SLC1A5-Mediated Glutamine Metabolism Through YY1.Cancer science · 2026Article
- Mechanisms of Metabolic Reprogramming Regulating Immunosuppression in the Gastric Cancer Tumor Microenvironment.Biomolecules · 2026Review
- Metabolic reprogramming networks in the gastric cancer tumor microenvironment: an integrated axis of nutrient competition, metabolic crosstalk, and immunosuppression.Frontiers in immunology · 2026Review
- Metabolic reprogramming as a key regulator in Helicobacter pylori-infected gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2026Review
- Exosome-mediated metabolic-immune regulatory axis: mechanisms of gastric cancer progression and resistance and targeting strategies.Frontiers in immunology · 2026Review
- Metabolic Reprogramming in Gastric Cancer Immunity Mechanisms and Therapeutic Implications.Oncology research · 2026Review
- Unveiling Metabolic Signatures as Potential Biomarkers in Common Cancers: Insights from Lung, Breast, Colorectal, Liver, and Gastric Tumours.Biomolecules · 2025Review
- The ATF4-glutamine axis: a central node in cancer metabolism, stress adaptation, and therapeutic targeting.Cell death discovery · 2025Review
- DRAM1 enhances the proliferation and metastasis of gastric cancer through the PI3K/AKT/mTOR signaling pathway and energy metabolism.Scientific reports · 2025Article
- Mendelian randomization analysis of plasma proteins reveals potential novel tumor markers for gastric cancer.Scientific reports · 2025Article
- NEK8 promotes the progression of gastric cancer by reprogramming asparagine metabolism.Molecular medicine (Cambridge, Mass.) · 2025Article
- Targeting amino acid metabolism to inhibit gastric cancer progression and promote anti-tumor immunity: a review.Frontiers in immunology · 2025Review
- Review
- Clinical significance of the tumor microenvironment on immune tolerance in gastric cancer.Frontiers in immunology · 2025Review
- Identification of a novel prognostic model for gastric cancer utilizing glutamine-related genes.Heliyon · 2024Article
- Glutamine and leukemia research: progress and clinical prospects.Discover oncology · 2024Review
- ASCT2 Regulates Fatty Acid Metabolism to Trigger Glutamine Addiction in Basal-like Breast Cancer.Cancers · 2024Article
- Progesterone inhibits endometrial cancer growth by inhibiting glutamine metabolism through ASCT2.Bioscience reports · 2024Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
purposeGlutamine (Gln) is essential for the proliferation of most cancer cells, making it an appealing target for cancer therapy. However, the role of Gln in gastric cancer (GC) metabolism is unknown and Gln-targeted therapy against GC remains scarce. The aim of this study was to investigate the relevance of Gln in GC growth and targeting.
methodsExpression of Gln transporter ASCT2 and glutamine synthetase (GS) in the parental and molecularly engineered GC cells or in human GC specimens was determined by RT-PCR and western blot analysis or immunohistochemistry. Cell proliferation and survival was assessed by CCK-8 assay and colony formation assay. Intracellular Gln content was measured by a HPLC system. Effects of ASCT2 and/or GS inhibitor on tumor growth were investigated in xenograft models.
resultsA significant heterogeneity of GC cells was observed with respect to their response to the treatment of ASCT2 inhibitor benzylserine (BenSer). Gln deprivation did not affect the BenSer-resistant cell growth due to endogenous GS expression, whose inhibition remarkably reduced cell proliferation. The differential in vitro sensitivity correlated with overall intracellular Gln content. Combined therapy with both ASCT2 and GS inhibitors produced a greater therapeutic efficacy than the treatment of either inhibitor alone. Furthermore, 77% human GC tissues were found to express moderate and high levels of ASCT2, 12% of which also co-expressed relatively high levels of GS.
conclusionGln mediates GC growth and the therapeutic efficacy of Gln-targeted treatment relies on distinct ASCT2 and GS expression pattern in specific gastric cancer groups.
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