ArticleCancer immunology, immunotherapy : CII2013
Endotoxin induces proliferation of NSCLC in vitro and in vivo: role of COX-2 and EGFR activation.
Article in Cancer immunology, immunotherapy : CII, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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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
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
- Relevance of humanized three-dimensional tumor tissue models: a descriptive systematic literature review.Cellular and molecular life sciences : CMLS · 2020Pooled it
- Porphyromonas gingivalis-derived lipopolysaccharide confers chemotherapy resistance and migratory ability on oral cancer cells by activating toll-like receptor 4 signaling pathway.Molecular biology reports · 2026Article
- The human microbiome in cancer: Not just a sidekick anymore.Genetics and molecular biology · 2026Article
- Microbiota-derived metabolites in tumorigenesis: mechanistic insights and therapeutic implications.Frontiers in pharmacology · 2025Review
- Marine Antimicrobial Peptide Epinecidin-1 Inhibits Proliferation Induced by Lipoteichoic acid and Causes cell Death in non-small cell lung cancer Cells via Mitochondria Damage.Probiotics and antimicrobial proteins · 2024Article
- Role of Lipopolysaccharides in the Inflammation and Pyroptosis of Alveolar Epithelial Cells in Acute Lung Injury and Acute Respiratory Distress Syndrome.Journal of inflammation research · 2024Review
- Lipopolysaccharide and lipoteichoic acid regulate the PI3K/AKT pathway through osteopontin/integrin β3 to promote malignant progression of non-small cell lung cancer.Journal of thoracic disease · 2023Article
- Toll-like receptor-guided therapeutic intervention of human cancers: molecular and immunological perspectives.Frontiers in immunology · 2023Review
- Add fuel to the fire: Inflammation and immune response in lung cancer combined with COVID-19.Frontiers in immunology · 2023Review
- Macrophages Release Extracellular Vesicles of Different Properties and Composition Following Exposure to Nanoparticles.International journal of molecular sciences · 2022Article
- Design and optimisation of a small-molecule TLR2/4 antagonist for anti-tumour therapy.RSC medicinal chemistry · 2021Article
- Article
- Ursolic Acid Protects Against Proliferation and Inflammatory Response in LPS-Treated Gastric Tumour Model and Cells by Inhibiting NLRP3 Inflammasome Activation.Cancer management and research · 2020Article
- Hydroxysafflor yellow A inhibited lipopolysaccharide-induced non-small cell lung cancer cell proliferation, migration, and invasion by suppressing the PI3K/AKT/mTOR and ERK/MAPK signaling pathways.Thoracic cancer · 2019Article
- Mig6 reduces inflammatory mediators production by regulating the activation of EGFR in LPS-induced endotoxemia.Journal of cellular physiology · 2018Article
- Targeting CREB-binding protein overrides LPS induced radioresistance in non-small cell lung cancer cell lines.Oncotarget · 2018Article
- Gram-negative bacteria facilitate tumor progression through TLR4/IL-33 pathway in patients with non-small-cell lung cancer.Oncotarget · 2018Article
- Roles of toll-like receptors: From inflammation to lung cancer progression.Biomedical reports · 2018Article
- The Role of PGEScientific reports · 2017Article
- IL-17C mediates the recruitment of tumor-associated neutrophils and lung tumor growth.Oncogene · 2017Article
Corrections and comments
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Authors and funding
17 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung cancer is frequently complicated by pulmonary infections which may impair prognosis of this disease. Therefore, we investigated the effect of bacterial lipopolysaccharides (LPS) on tumor proliferation in vitro in the non-small cell lung cancer (NSCLC) cell line A549, ex vivo in a tissue culture model using human NSCLC specimens and in vivo in the A549 adenocarcinoma mouse model. LPS induced a time- and dose-dependent increase in proliferation of A549 cells as quantified by MTS activity and cell counting. In parallel, an increased expression of the proliferation marker Ki-67 and cyclooxygenase (COX)-2 was detected both in A549 cells and in ex vivo human NSCLC tissue. Large amounts of COX-2-derived prostaglandin (PG)E(2) were secreted from LPS-stimulated A549 cells. Pharmacological interventions revealed that the proliferative effect of LPS was dependent on CD14 and Toll-like receptor (TLR)4. Moreover, blocking of the epidermal growth factor receptor (EGFR) also decreased LPS-induced proliferation of A549 cells. Inhibition of COX-2 activity in A549 cells severely attenuated both PGE(2) release and proliferation in response to LPS. Synthesis of PGE(2) was also reduced by inhibiting CD14, TLR4 and EGFR in A549 cells. The proliferative effect of LPS on A549 cells could be reproduced in the A549 adenocarcinoma mouse model with enhancement of tumor growth and Ki-67 expression in implanted tumors. In summary, LPS induces proliferation of NSCLC cells in vitro, ex vivo in human NSCLC specimen and in vivo in a mouse model of NSCLC. Pulmonary infection may thus directly induce tumor progression in NSCLC.
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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.