ArticleJournal for immunotherapy of cancer2021
GCH1 induces immunosuppression through metabolic reprogramming and IDO1 upregulation in triple-negative breast cancer.
Article in Journal for immunotherapy of cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 54 citations in OpenAlex.
- Article
- TET1 as a master regulator controlling GPX4-dependent and -independent ferroptosis surveillance in acute myeloid leukemia.Nature communications · 2026Article
- Ferroptosis in biliary tract cancer: Molecular mechanisms and therapeutic applications (Review).International journal of oncology · 2026Review
- Discovering the abnormalities and functional importance of ferroptosis-related molecules in cervical cancer.International journal of medical sciences · 2026Article
- Role of Tryptophan Metabolism in Cancer.Cancer innovation · 2025Review
- Recent progress in immune evasion mechanisms of triple-negative breast cancer.Journal of translational medicine · 2025Review
- Monod: model-based discovery and integration through fitting stochastic transcriptional dynamics to single-cell sequencing data.Nature methods · 2025Article
- Review
- Gambogenic Acid Suppresses Malignant Progression of Non-Small Cell Lung Cancer via GCH1-Mediated Ferroptosis.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Cross-species RNAi therapy via AAV delivery alleviates neuropathic pain by targeting GCH1.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Prognostic significance of the inhibitory-to-stimulatory immune checkpoint ratio in patients with breast cancer.Frontiers in oncology · 2025Article
- Multi-omics analyses construct an inflammatory response based prognostic gene signature for cervical cancer and suggest tumor infiltrating monocytes subgroups as key players.Frontiers in immunology · 2025Article
- Identifying compound-protein interactions with knowledge graph embedding of perturbation transcriptomics.Cell genomics · 2024Article
- Role of indoleamine 2, 3-dioxygenase 1 in immunosuppression of breast cancer.Cancer pathogenesis and therapy · 2024Review
- Ferroptosis: a new hunter of hepatocellular carcinoma.Cell death discovery · 2024Review
- Lactylation-related gene signature for prognostic prediction and immune infiltration analysis in breast cancer.Heliyon · 2024Article
- The role of metabolic reprogramming in immune escape of triple-negative breast cancer.Frontiers in immunology · 2024Review
- New role for GCH1 in cancer.Translational breast cancer research : a journal focusing on translational research in breast cancer · 2024Article
- Metronomic chemotherapy in cancer treatment: new wine in an old bottle.Theranostics · 2024Review
- Nanodelivery Optimization of IDO1 Inhibitors in Tumor Immunotherapy: Challenges and Strategies.International journal of nanomedicine · 2024Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeRegulatory T cells (Tregs) heavily infiltrate triple-negative breast cancer (TNBC), and their accumulation is affected by the metabolic reprogramming in cancer cells. In the present study, we sought to identify cancer cell-intrinsic metabolic modulators correlating with Tregs infiltration in TNBC. EXPERIMENTAL
designUsing the RNA-sequencing data from our institute (n=360) and the Molecular Taxonomy of Breast Cancer International Consortium TNBC cohort (n=320), we calculated the abundance of Tregs in each sample and evaluated the correlation between gene expression levels and Tregs infiltration. Then,
resultsWe revealed that GTP cyclohydrolase 1 (
conclusionsTumor-cell-intrinsic GCH1 induced immunosuppression through metabolic reprogramming and IDO1 upregulation in TNBC. Inhibition of GCH1 by DAHP serves as a potential immunometabolic strategy in TNBC.
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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.