ArticleCell communication and signaling : CCS2024
The immune checkpoint TIGIT/CD155 promotes the exhaustion of CD8 + T cells in TNBC through glucose metabolic reprogramming mediated by PI3K/AKT/mTOR signaling.
Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 46 citations in OpenAlex.
- The tumor-microenvironment-associated prognostic gene TIGIT promotes malignant phenotypes in esophageal carcinoma.Translational oncology · 2026Article
- Endogenous CD155 drives metabolic reprogramming via PI3K/AKT/HIF-1α-glycolysis axis to mediate anti-PD-1 resistance in non-small cell lung cancer.Clinical and translational medicine · 2026Article
- Artemisinin liposomes regulates breast cancer metastasis and apoptosis through TIGIT/CD155 signal axis.Apoptosis : an international journal on programmed cell death · 2026Article
- Metabolic enzymes and immune receptors as emerging checkpoints in breast cancer: mechanisms, clinical trials, and therapeutic implications.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- SerpinB7 promotes c-Myc-mediated glycolysis by interacting with ANXA2 to facilitate the progression of non-small cell lung cancer.Molecular cancer · 2026Article
- Ferroptosis-related gene EPAS1 suppresses breast cancer progression by inhibiting M2 macrophage polarization.Discover oncology · 2026Article
- Targeting the HMGB1-IL32 pathway to alleviate T cell exhaustion in epithelial ovarian cancer.GeroScience · 2026Article
- CD155 and its receptors in glioma: prospects for emerging immune checkpoint inhibitors.Acta neuropathologica communications · 2026Review
- Epithelial CD155-TIGIT/CD226 signaling links CD8⁺ T-cell exhaustion to frequent exacerbations in COPD.Respiratory research · 2026Observational
- From guardians to traitors: molecular mechanisms of tumor-induced T cell betrayal.Molecular cancer · 2026Review
- Integrated single-cell and bulk RNA sequencing reveals novel biomarkers of invasive adenocarcinoma subtypes in lung adenocarcinoma.Translational cancer research · 2026Article
- Macrophage metabolic reprogramming by vanadium released from glucose-responsive bio-gel accelerates diabetic wound repair.Signal transduction and targeted therapy · 2026Article
- T‑Cell Immunoreceptor with Ig and Immunoreceptor Tyrosine-Based Inhibitory Motif Domains/Cluster of Differentiation 40 Cellular Nanovesicles Carrying Oxaliplatin Exhibited Superior Pancreatic Cancer Cells Therapy.ACS pharmacology & translational science · 2026Article
- T-Cell Profiles in HBV Functional Cure and People Living With HIV: Known Knowns, Known Unknowns, and Unknown Unknowns.Current HIV/AIDS reports · 2026Review
- Exploring the role of metabolic disorders and gut microbiome in immune checkpoint regulation in cancer: PI3K/AKT/mTOR focus.Journal of physiology and biochemistry · 2026Review
- Proliferative Tumor States and Immunogenic Ecosystems Predict Neoadjuvant Chemotherapy Response in Triple-Negative Breast Cancer.Biomedicines · 2026Article
- XOR-mediated tumor-selective nanomaterial therapy: achieving tumor and immune cell dual regulation through intracellular ROS generation.Journal of nanobiotechnology · 2026Article
- T Cell Exhaustion in Hepatocellular Carcinoma: A Substantial Barrier in Immunotherapy.Journal of cellular and molecular medicine · 2026Review
- Article
- Association of TIGIT and CD155 with KRAS, NRAS, BRAF, PIK3CA, and AKT Gene Mutations, MSI Status, and Cytokine Profiles in Colorectal Cancer.International journal of molecular sciences · 2026Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
objectiveThe CD155/TIGIT axis has attracted considerable interest as an emerging immune checkpoint with potential applications in cancer immunotherapy. Our research focused on investigating the role of CD155/TIGIT checkpoints in the progression of triple-negative breast cancer (TNBC).
methodsWe evaluated CD155 and TIGIT expression in TNBC tissues using both immunohistochemistry (IHC) and gene expression profiling. Our experiments, both in vivo and in vitro, provided evidence that inhibiting the CD155/TIGIT pathway reinstates the ability of CD8 + T cells to generate cytokines. To assess the impact of CD155/TIGIT signaling blockade, we utilized Glucose Assay Kits and Lactate Assay Kits to measure alterations in glucose and lactate levels within CD8 + T cells. We employed western blotting (WB) to investigate alterations in glycolytic-related proteins within the PI3K/AKT/mTOR pathways following the inhibition of CD155/TIGIT signaling.
resultsCD155 exhibits heightened expression within TNBC tissues and exhibits a negative correlation with the extent of infiltrating CD8 + T cells. Furthermore, patients with TNBC demonstrate elevated levels of TIGIT expression. Our findings indicate that the interaction between CD155 and TIGIT disrupts the glucose metabolism of CD8 + T cells by suppressing the activation of the PI3K/AKT/mTOR signaling pathway, ultimately leading to the reduced production of cytokines by CD8 + T cells. Both in vivo and in vitro experiments have conclusively demonstrated that the inhibition of CD155/TIGIT interaction reinstates the capacity of CD8 + T cells to generate cytokines. Moreover, in vivo administration of the blocking antibody against TIGIT not only inhibits tumor growth but also augments the functionality of CD8 + T lymphocytes.
conclusionsOur research findings strongly suggest that CD155/TIGIT represents a promising therapeutic target for treating 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.