ArticleCancer science2010
TLR3 induction by anticancer drugs potentiates poly I:C-induced tumor cell apoptosis.
Article in Cancer science, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 68 citations in OpenAlex.
- Poly(I:C) Lipoamino Bundle LNPs Induce Tumor Cytotoxicity and Immune Activation with Enhanced Efficacy by Survivin Silencing.International journal of molecular sciences · 2026Article
- TL-532, a novel specific Toll-like receptor 3 agonist rationally designed for targeting cancers: discovery process and biological characterization.Microbial cell (Graz, Austria) · 2023Article
- p53 signaling in cancer progression and therapy.Cancer cell international · 2021Review
- Toll-Like Receptor-Based Strategies for Cancer Immunotherapy.Journal of immunology research · 2021Review
- Tackling Immune Targets for Breast Cancer: Beyond PD-1/PD-L1 Axis.Frontiers in oncology · 2021Review
- Catecholamines suppress fatty acid re-esterification and increase oxidation in white adipocytes via STAT3.Nature metabolism · 2020Article
- P53: A Guardian of Immunity Becomes Its Saboteur through Mutation.International journal of molecular sciences · 2020Review
- Review
- Interferon regulatory factor 3 plays a role in macrophage responses to interferon-γ.Immunobiology · 2019Article
- Ingestion of Non-digestible Carbohydrates From Plant-Source Foods and Decreased Risk of Colorectal Cancer: A Review on the Biological Effects and the Mechanisms of Action.Frontiers in nutrition · 2019Review
- Exploiting poly(I:C) to induce cancer cell apoptosis.Cancer biology & therapy · 2017Review
- Double-stranded RNA induces chicken T-cell lymphoma apoptosis by TRIF and NF-κB.Scientific reports · 2017Article
- Ligand dependent restoration of human TLR3 signaling and death in p53 mutant cells.Oncotarget · 2016Article
- Highly activated p53 contributes to selectively increased apoptosis of latently HIV-1 infected cells upon treatment of anticancer drugs.Virology journal · 2016Article
- Modulation of Toll-like receptor signaling in innate immunity by natural products.International immunopharmacology · 2016Review
- Dysregulation of signaling pathways associated with innate antibacterial immunity in patients with pancreatic cancer.Central-European journal of immunology · 2016Review
- Endoplasmic Reticulum (ER) Stress Induces Sirtuin 1 (SIRT1) Expression via the PI3K-Akt-GSK3β Signaling Pathway and Promotes Hepatocellular Injury.The Journal of biological chemistry · 2015Article
- MUC1 regulates epithelial inflammation and apoptosis by PolyI:C through inhibition of Toll/IL-1 receptor-domain-containing adapter-inducing IFN-β (TRIF) recruitment to Toll-like receptor 3.American journal of respiratory cell and molecular biology · 2014Article
- Article
- TLR agonists: our best frenemy in cancer immunotherapy.Journal of leukocyte biology · 2013Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Toll-like receptor 3 (TLR3) has gained recognition as a novel molecular target for cancer therapy because TLR3 activation by its synthetic ligand poly I:C directly causes tumor cell death. Recently, we reported that tumor suppressor p53 increases the expression of TLR3 in several tumor cell lines. Another study also showed that interferon-alpha (IFN-alpha) up-regulates TLR3 expression. We thus hypothesized that various anticancer drugs such as p53-activating reagents and IFNs may potentiate poly I:C-induced tumor cell death through the up-regulation of TLR3 expression. Here, we screened several anticancer drugs that, together with poly I:C, effectively cause tumor cell death in colon carcinoma HCT116 cells. We found that the DNA-damaging reagent 5-fluorouracil (5-FU) increased TLR3 mRNA expression and potentiated poly I:C-induced apoptosis in HCT116 p53(+/+) cells but had only minimal effect in p53(-/-) cells, indicating a p53-dependent pathway. On the other hand, IFN-alpha increased poly I:C-induced apoptosis and the TLR3 mRNA level in HCT116 p53(+/+) and p53(-/-) cell lines. Furthermore, the combination of poly I:C, 5-FU and IFN-alpha induced the highest apoptosis in HCT116 p53(+/+) and p53(-/-) cells. Taken together, these data suggest that the anticancer drugs increased TLR3 expression and subsequently potentiated poly I:C-induced apoptosis likely via p53-dependent and -independent pathways. Considering that the p53 status in malignant cells is heterogeneous, this combination approach may provide a highly effective tumor therapy.
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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.