ReviewCancer biology & therapy2017
Exploiting poly(I:C) to induce cancer cell apoptosis.
Review in Cancer biology & therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
What it found
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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.
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Who cites it
79 citing papers in PubMed, 122 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
- Identification of poly(I:C) interacted proteins and their regulation in transcription level against bacterial infection in zebrafish.Frontiers in immunology · 2026Article
- Key role of TLR3 in type I IFN expression and apoptosis induction in IBDV-infected chicken fibroblast cells.Frontiers in cellular and infection microbiology · 2026Article
- EGFR-targeted affibody-polyIC polyplex kills EGFR-overexpressing cancer cells without activating the EGFR.PloS one · 2026Article
- Downregulation of Engulfment and cell motility 1 (Elmo1) induces quiescence and resistance to poly(I:C)-induced apoptosis in endothelial cells.Cell death & disease · 2025Article
- MyD88 Contributes to TLR3-Mediated NF-κB Activation and Cytokine Production in Macrophages.Cells · 2025Article
- Genistein enhances TLR3-mediated apoptosis and immune signaling in breast cancer cells.Medical oncology (Northwood, London, England) · 2025Article
- Exploring the Role of Pattern Recognition Receptors as Immunostimulatory Molecules.Immunity, inflammation and disease · 2025Review
- Inorganic Arsenic Induces Elevated p53 Levels with Altered Functionality Impacting the Expression of Toll-like Receptor 3 and Other Target Genes in Immortalized Prostate Epithelial Cells.International journal of molecular sciences · 2025Article
- Interaction of Selected Anthracycline and Tetracycline Chemotherapeutics with Poly(I:C) Molecules.ACS omega · 2025Article
- Spermidine as a Potential Protective Agents Against Poly(I:C)-Induced Immune Response, Oxidative Stress, Apoptosis, and Testosterone Decrease in Yak Leydig Cells.International journal of molecular sciences · 2025Article
- Regulation of immune responses by a tumor necrosis factor in pearl oysters: insights fromActa biochimica et biophysica Sinica · 2025Article
- Optimizing rWTC-MBTA Vaccine Formulations, Dosing Regimens, and Cryopreservation Techniques to Enhance Anti-Metastatic Immunotherapy.International journal of molecular sciences · 2025Article
- Implications of Raftlin in different diseases: from molecular biology to diagnostic value.Biomarkers in medicine · 2025Review
- Differences in Susceptibility to SARS-CoV-2 Infection Among Transgenic hACE2-Hamster Founder Lines.Viruses · 2024Article
- Pig Milk Exosome Packaging ssc-miR-22-3p Alleviates Pig Intestinal Epithelial Cell Injury and Inflammatory Response by TargetingInternational journal of molecular sciences · 2024Article
- Poly I: C Alleviated Duck Intestinal Injury Infected with Duck Viral Enteritis by Inhibiting Apoptosis.Current microbiology · 2024Article
- Article
- Lipid Nanoparticle Encapsulation Empowers Poly(I:C) to Activate Cytoplasmic RLRs and Thereby Increases Its Adjuvanticity.Small (Weinheim an der Bergstrasse, Germany) · 2024Article
- When inflammatory stressors dramatically change, disease phenotypes may transform between autoimmune hematopoietic failure and myeloid neoplasms.Frontiers in immunology · 2024Review
19 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TLR3 belong to the Toll-like receptors family, it is mainly expressed on immune cells where it senses pathogen-associated molecular patterns and initiates innate immune response. TLR3 agonist poly(I:C) was developed to mimic pathogens infection and boost immune system activation to promote anti-cancer therapy. Accordingly, TLR agonists were included in the National Cancer Institute list of immunotherapeutic agents with the highest potential to cure cancer. Besides well known effects on immune cells, poly(I:C) was also shown, in experimental models, to directly induce apoptosis in cancer cells expressing TLR3. This review presents the current knowledge on the mechanism of poly(I:C)-induced apoptosis in cancer cells. Experimental evidences on positive or negative regulators of TLR3-mediated apoptosis induced by poly(I:C) are reported and strategies are proposed to successfully promote this event in cancer cells. Cancer cells apoptosis is an additional arm offered by poly(I:C), besides activation of immune system, for the treatment of various type of cancer. A further dissection of TLR3 signaling would contribute to greater resolution of the critical steps that impede full exploitation of the poly(I:C)-induced apoptosis. Experimental evidences about negative regulator of poly(I:C)-induced apoptotic program should be considered in combinations with TLR3 agonists in clinical trials.
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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.