ArticleOncotarget2016
Stimulation of the toll-like receptor 3 promotes metabolic reprogramming in head and neck carcinoma cells.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- Toll-like Receptor 3 as a Context-Dependent Molecular Switch in Epithelial Cancers: Balancing Cell Death and Tumor-Supportive Programs.International journal of molecular sciences · 2026Review
- Metabolic Plasticity and Cancer Stem Cell Metabolism: Exploring the Glycolysis-OXPHOS Switch as a Mechanism for Resistance and Tumorigenesis.Stem cell reviews and reports · 2025Review
- Targeting DAMPs by Aspirin Inhibits Head and Neck Cancer Stem Cells and Stimulates Radio-Sensitization to Proton Therapy.Cancers · 2025Article
- The crosstalk between senescence, tumor, and immunity: molecular mechanism and therapeutic opportunities.MedComm · 2025Review
- Mithramycin targets head and neck cancer stem cells by inhibiting Sp1 and UFMylation.Cancer cell international · 2024Article
- Necrotic Cells from Head and Neck Carcinomas Release Biomolecules That Are Activating Toll-like Receptor 3.International journal of molecular sciences · 2023Article
- Palmitic acid combined with γ-interferon inhibits gastric cancer progression by modulating tumor-associated macrophages' polarization via the TLR4 pathway.Journal of cancer research and clinical oncology · 2023Article
- Dialog beyond the Grave: Necrosis in the Tumor Microenvironment and Its Contribution to Tumor Growth.International journal of molecular sciences · 2023Review
- Innate and Adaptive Responses of Intratumoral Immunotherapy with Endosomal Toll-Like Receptor Agonists.Biomedicines · 2022Review
- Context-dependent functions of pattern recognition receptors in cancer.Nature reviews. Cancer · 2022Review
- Cysteine cathepsin C: a novel potential biomarker for the diagnosis and prognosis of glioma.Cancer cell international · 2022Article
- Harnessing Metabolic Reprogramming to Improve Cancer Immunotherapy.International journal of molecular sciences · 2021Review
- A New Lectin fromBioMed research international · 2021Article
- Toll-like receptors (TLRs): An old family of immune receptors with a new face in cancer pathogenesis.Journal of cellular and molecular medicine · 2021Review
- Review
- Senescent T cells within suppressive tumor microenvironments: emerging target for tumor immunotherapy.The Journal of clinical investigation · 2020Review
- Radio-sensitization of head and neck cancer cells by a combination of poly(I:C) and cisplatin through downregulation of survivin and c-IAP2.Cellular oncology (Dordrecht, Netherlands) · 2019Article
- Genetic variant of IRAK2 in the toll-like receptor signaling pathway and survival of non-small cell lung cancer.International journal of cancer · 2018Article
- TLR-mediated metabolic reprogramming in the tumor microenvironment: potential novel strategies for cancer immunotherapy.Cellular & molecular immunology · 2018Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 10 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study, a possible link between the innate immune recognition receptor TLR3 and metabolic reprogramming in Head and Neck carcinoma (HNC) cells was investigated. The effects of TLR3 stimulation/knock-down were assessed under several culture conditions in 4 HNC cell-lines by cell growth assays, targeted metabolomics, and glycolysis assays based on time-resolved analysis of proton release (Seahorse analyzer). The stimulation of TLR3 by its synthetic agonist Poly(A:U) resulted in a faster growth of HNC cells under low foetal calf serum conditions. Targeted analysis of glucose metabolism pathways demonstrated a tendency towards a shift from tricarboxylic acid cycle (Krebs cycle) to glycolysis and anabolic reactions in cells treated with Poly(A:U). Glycolysis assays confirmed that TLR3 stimulation enhanced the capacity of malignant cells to switch from oxidative phosphorylation to extra-mitochondrial glycolysis. We found evidence that HIF-1α is involved in this process: addition of the TLR3 agonist resulted in a higher cell concentration of the HIF-1α protein, even in normoxia, whereas knocking-down TLR3 resulted in a lower concentration, even in hypoxia. Finally, we assessed TLR3 expression by immunohistochemistry in a series of 7 HNSCC specimens and found that TLR3 was detected at higher levels in tumors displaying a hypoxic staining pattern. Overall, our results demonstrate that TLR3 stimulation induces the Warburg effect in HNC cells in vitro, and suggest that TLR3 may play a role in tumor adaptation to hypoxia.
Indexed as
Identifiers
What OpenQuestion holds
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.