ArticleCancer immunology research2015
Cytotoxic T lymphocytes block tumor growth both by lytic activity and IFNγ-dependent cell-cycle arrest.
Article in Cancer immunology research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 1 of them a synthesis that pooled it.
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Who cites it
77 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.
- Type I T cells sensitize treatment refractory tumors to chemotherapy through inhibition of oncogenic signaling pathways.Journal for immunotherapy of cancer · 2021Pooled it
- Adaptive resistance in cancer immunotherapy.Cellular & molecular immunology · 2026Review
- Mathematical modeling of immune counter-regulation predicts efficacy of fractionated CD8Scientific reports · 2026Article
- Harnessing Inflammatory Monocytes to Overcome Resistance to Anti-PD-1 Immunotherapy.bioRxiv : the preprint server for biology · 2026Article
- CAR-T cells co-expressing IL-7 and CCL19 promote epitope spreading to enhance antitumor immunity.Cancer immunology, immunotherapy : CII · 2026Article
- STING agonism in brain tumours: mechanisms, challenges, and therapeutic advances.Frontiers in oncology · 2026Review
- Anlotinib Combined with Programmed Death-1/Programmed Death-Ligand 1 Inhibitor 9 Hydrochloride Suppresses Colorectal Cancer Progression by Inducing Neovascularization and Reprogramming the Tumor Immune Microenvironment in MSS Murine Model.ImmunoTargets and therapy · 2026Article
- Genome instability and crosstalk with the immune response.Genome medicine · 2025Review
- The difference in tumor immune microenvironment and IFN-γ response between solid and non-solid adenocarcinoma.Translational lung cancer research · 2025Article
- Lung adenocarcinoma-derived IFN-γ promotes growth by modulating CD8+ T cell production of CCR5 chemokines.The Journal of clinical investigation · 2025Article
- Dual role of interferon-gamma in the response of melanoma patients to immunotherapy with immune checkpoint inhibitors.Molecular cancer · 2025Review
- Contribution of tumor microenvironment (TME) to tumor apoptosis, angiogenesis, metastasis, and drug resistance.Medical oncology (Northwood, London, England) · 2025Review
- Identification of three subtypes of thyroid cancer based on IFN-γ-related genes to reveal their prognostic characteristics.Langenbeck's archives of surgery · 2025Article
- Article
- Ferroptosis contributes to immunosuppression.Frontiers of medicine · 2025Review
- An Immunoinformatic Approach for Identifying and Designing Conserved Multi-Epitope Vaccines for Coronaviruses.Biomedicines · 2024Article
- Spatiotemporal transcriptomic profiling and modeling of mouse brain at single-cell resolution reveals cell proximity effects of aging and rejuvenation.bioRxiv : the preprint server for biology · 2024Article
- Non-canonical deubiquitination of OTUB1 induces IFNγ-mediated cell cycle arrest via regulation of p27 stability.Oncogene · 2024Article
- SOX10 Loss Sensitizes Melanoma Cells to Cytokine-Mediated Inflammatory Cell Death.Molecular cancer research : MCR · 2024Article
- TL1A induces apoptosis via DR3 in grass carp (Fish and shellfish immunology reports · 2023Article
17 more citing papers are in PubMed but not listed here.
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10 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To understand global effector mechanisms of CTL therapy, we performed microarray gene expression analysis in a murine model using pmel-1 T-cell receptor (TCR) transgenic T cells as effectors and B16 melanoma cells as targets. In addition to upregulation of genes related to antigen presentation and the MHC class I pathway, and cytotoxic effector molecules, cell-cycle-promoting genes were downregulated in the tumor on days 3 and 5 after CTL transfer. To investigate the impact of CTL therapy on the cell cycle of tumor cells in situ, we generated B16 cells expressing a fluorescent ubiquitination-based cell-cycle indicator (B16-fucci) and performed CTL therapy in mice bearing B16-fucci tumors. Three days after CTL transfer, we observed diffuse infiltration of CTLs into the tumor with a large number of tumor cells arrested at the G1 phase of the cell cycle, and the presence of spotty apoptotic or necrotic areas. Thus, tumor growth suppression was largely dependent on G1 cell-cycle arrest rather than killing by CTLs. Neutralizing antibody to IFNγ prevented both tumor growth inhibition and G1 arrest. The mechanism of G1 arrest involved the downregulation of S-phase kinase-associated protein 2 (Skp2) and the accumulation of its target cyclin-dependent kinase inhibitor p27 in the B16-fucci tumor cells. Because tumor-infiltrating CTLs are far fewer in number than the tumor cells, we propose that CTLs predominantly regulate tumor growth via IFNγ-mediated profound cytostatic effects rather than via cytotoxicity. This dominance of G1 arrest over other mechanisms may be widespread but not universal because IFNγ sensitivity varied among tumors.
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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.