ArticleFrontiers in immunology2023
Toll-like receptors 2, 4, and 9 modulate promoting effect of COPD-like airway inflammation on K-ras-driven lung cancer through activation of the MyD88/NF-ĸB pathway in the airway epithelium.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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19 citing papers in PubMed, 23 citations in OpenAlex.
- Myeloid TLR2 signaling amplifies immunopathology in influenza-infected murine neonates.American journal of respiratory cell and molecular biology · 2026Article
- Loss of the RAGE function in hypoxic conditions exacerbates the malignant progression of lung adenocarcinoma via damage-associated molecular pattern signaling.Translational oncology · 2026Article
- IntratumoralAnimals : an open access journal from MDPI · 2026Article
- Toll-Like Receptors in the Immunotherapy Era: Dual-Edged Swords of Tumor Immunity and Clinical Translation.MedComm · 2025Review
- Exploring the metabolomics and metagenomics of chronic obstructive pulmonary disease (COPD) and lung cancer: unraveling the complex interplay.Journal of thoracic disease · 2025Review
- Phosphorylated Toll-like receptor 3 nuclear translocation in cancer cell promotes metastasis and chemoresistance.Signal transduction and targeted therapy · 2025Article
- Hederasaponin C ameliorates chronic obstructive pulmonary disease pathogenesis by targeting TLR4 to inhibit NF-κB/MAPK signaling pathways.Chinese medicine · 2025Article
- Article
- Antitumor activity of gamma-irradiated Rosa canina L. against lung carcinoma in rat model: a proposed mechanism.BMC complementary medicine and therapies · 2025Article
- Targeting the Toll-like Receptor Signaling Pathway in Lung Cancer: Therapeutic Opportunities and Challenges.Current drug targets · 2025Review
- Targeting Non-Eosinophilic Immunological Pathways in COPD and AECOPD: Current Insights and Therapeutic Strategies.International journal of chronic obstructive pulmonary disease · 2025Review
- Potential role of lactylation in intrinsic immune pathways in lung cancer.Frontiers in pharmacology · 2025Review
- Pyroptosis for osteoarthritis treatment: insights into cellular and molecular interactions inflammatory.Frontiers in immunology · 2025Review
- Impact of asthma and/or chronic obstructive pulmonary disease on the survival of patients with lung adenocarcinoma.Therapeutic advances in medical oncology · 2025Article
- Innate immunity in tumors: roles and therapeutic targets.Frontiers in immunology · 2025Review
- Premalignant Progression in the Lung: Knowledge Gaps and Novel Opportunities for Interception of Non-Small Cell Lung Cancer. An Official American Thoracic Society Research Statement.American journal of respiratory and critical care medicine · 2024Review
- Toll-like Receptors: Key Players in Squamous Cell Carcinoma Progression.Journal of clinical medicine · 2024Article
- Dark under the Lamp: Neglected Biological Pollutants in the Environment Are Closely Linked to Lung Cancer.International journal of molecular sciences · 2024Review
- Pan-Cancer Analysis and Validation of Opioid-Related Receptors Reveals the Immunotherapeutic Value of Toll-Like Receptor 4.International journal of general medicine · 2023Article
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Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
Abstract
Introduction: Toll-like receptors (TLRs) are an extensive group of proteins involved in host defense processes that express themselves upon the increased production of endogenous damage-associated molecular patterns (DAMPs) and pathogen-associated molecular patterns (PAMPs) due to the constant contact that airway epithelium may have with pathogenic foreign antigens. We have previously shown that COPD-like airway inflammation induced by exposure to an aerosolized lysate of nontypeable Methods: In the present study, we have dissected the role of TLRs in this process by knocking out TLR2, 4, and 9 and analyzing how these deletions affect the promoting effect of COPD-like airway inflammation on K-ras-driven lung adenocarcinoma. Results: We found that knockout of TLR 2, 4, or 9 results in a lower tumor burden, reduced angiogenesis, and tumor cell proliferation, accompanied by increased tumor cell apoptosis and reprogramming of the tumor microenvironment to one that is antitumorigenic. Additionally, knocking out of downstream signaling pathways, MyD88/NF-κB in the airway epithelial cells further recapitulated this initial finding. Discussion: Our study expands the current knowledge of the roles that TLR signaling plays in lung cancer, which we hope, can pave the way for more reliable and efficacious prevention and treatment modalities for lung cancer.
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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.