ArticleThe Journal of biological chemistry2017
Surface Toll-like receptor 3 expression in metastatic intestinal epithelial cells induces inflammatory cytokine production and promotes invasiveness.
Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 60 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
- P2YJournal of immunology research · 2026Article
- Toll-like receptors: versatile players in tumor.Frontiers in immunology · 2026Review
- Immune and Stem Cell Interactions in Periodontal Disease: The Regulatory Role of Toll-Like Receptor 3.Advances in experimental medicine and biology · 2026Review
- UNC93B1: a novel immune-related prognostic biomarker in breast cancer.Discover oncology · 2025Article
- Cell surface RNA biology: new roles for RNA binding proteins.Trends in biochemical sciences · 2025Review
- Research progress and strategies for vaccines and targeted drugs against highly virulent porcine epidemic diarrhea virus.Frontiers in microbiology · 2025Review
- TLR3 activation mediates partial epithelial-to-mesenchymal transition in human keratinocytes.Life science alliance · 2024Article
- Immunity and Coagulation in COVID-19.International journal of molecular sciences · 2024Review
- Strategies for treating the cold tumors of cholangiocarcinoma: core concepts and future directions.Clinical and experimental medicine · 2024Review
- Comparative network-based analysis of toll-like receptor agonist, L-pampo signaling pathways in immune and cancer cells.Scientific reports · 2024Article
- Sub-Chronic Methomyl Exposure Induces Oxidative Stress and Inflammatory Responses in Zebrafish with Higher Female Susceptibility.Antioxidants (Basel, Switzerland) · 2024Article
- Synergistic Inhibitory Effect of Lactobacillus Cell Lysates and Butyrate on Poly I:C-Induced IL-8 Production in Human Intestinal Epithelial Cells.Probiotics and antimicrobial proteins · 2024Article
- Necrotic Cells from Head and Neck Carcinomas Release Biomolecules That Are Activating Toll-like Receptor 3.International journal of molecular sciences · 2023Article
- Genetic heterogeneity of colorectal cancer and the microbiome.World journal of gastrointestinal oncology · 2023Review
- Dialog beyond the Grave: Necrosis in the Tumor Microenvironment and Its Contribution to Tumor Growth.International journal of molecular sciences · 2023Review
- Microbiota of the gastrointestinal tract: Friend or foe?World journal of gastroenterology · 2023Review
- A β-Cyclodextrin-Based Nanoparticle with Very High Transfection Efficiency Unveils siRNA-Activated TLR3 Responses in Human Prostate Cancer Cells.Pharmaceutics · 2022Article
- Human Milk Oligosaccharide 2'-Fucosyllactose Modulates Local Viral Immune Defense by Supporting the Regulatory Functions of Intestinal Epithelial and Immune Cells.International journal of molecular sciences · 2022Article
- Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Toll-like receptors (TLRs) are innate immune receptors for sensing microbial molecules and damage-associated molecular patterns released from host cells. Double-stranded RNA and the synthetic analog polyinosinic:polycytidylic acid (poly(I:C)) bind and activate TLR3. This stimulation leads to recruitment of the adaptor molecule TRIF (Toll/IL-1 resistance (TIR) domain-containing adapter-inducing interferon β) and activation of the transcription factors nuclear factor κB (NF-κB) and interferon regulatory factor 3 (IRF-3), classically inducing IFNβ production. Here we report that, unlike non-metastatic intestinal epithelial cells (IECs), metastatic IECs express TLR3 and that TLR3 promotes invasiveness of these cells. In response to poly(I:C) addition, the metastatic IECs also induced the chemokine CXCL10 in a TLR3-, TRIF-, and IRF3-dependent manner but failed to produce IFNβ. This was in contrast to healthy and non-metastatic IECs, which did not respond to poly(I:C) stimulation. Endolysosomal acidification and the endosomal transporter protein UNC93B1 was required for poly(I:C)-induced CXCL10 production. However, TLR3-induced CXCL10 was triggered by immobilized poly(I:C), was only modestly affected by inhibition of endocytosis, and could be blocked with an anti-TLR3 antibody, indicating that TLR3 can still signal from the cell surface of these cells. Furthermore, plasma membrane fractions from metastatic IECs contained both full-length and cleaved TLR3, demonstrating surface expression of both forms of TLR3. Our results imply that metastatic IECs express surface TLR3, allowing it to sense extracellular stimuli that trigger chemokine responses and promote invasiveness in these cells. We conclude that altered TLR3 expression and localization may have implications for cancer progression.
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