ArticleThoracic cancer2015
Novel link between prostaglandin E2 (PGE2) and cholinergic signaling in lung cancer: The role of c-Jun in PGE2-induced α7 nicotinic acetylcholine receptor expression and tumor cell proliferation.
Article in Thoracic cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Neutrophils in non-small cell lung cancer and immunotherapy with PD-1/PD-L1 inhibitors.Journal of translational medicine · 2025Review
- The role of acetylcholine and its receptors in tumor immune regulation: mechanisms and potential therapeutic targets.Molecular cancer · 2025Review
- Role of nitric oxide, prostaglandins, thromboxanes and endothelins in lung cancer: An overview.World journal of clinical cases · 2025Review
- COX-2 in lung cancer: Mechanisms, development, and targeted therapies.Chronic diseases and translational medicine · 2024Review
- Targeting Alpha7 Nicotinic Acetylcholine Receptors in Lung Cancer: Insights, Challenges, and Therapeutic Strategies.ACS pharmacology & translational science · 2024Review
- Omega-6 Polyunsaturated Fatty Acids Enhance Tumor Aggressiveness in Experimental Lung Cancer Model: Important Role of Oxylipins.International journal of molecular sciences · 2022Article
- PACER lncRNA regulates COX-2 expression in lung cancer cells.Oncotarget · 2022Article
- Intranasal Administration ofInternational journal of molecular sciences · 2021Article
- Indomethacin Treatment Post-irradiation Improves Mouse Parotid Salivary Gland Function via Modulation of Prostaglandin EFrontiers in bioengineering and biotechnology · 2021Article
- Inhibition of PI3K-AKT Signaling Blocks PGEOncoTargets and therapy · 2020Article
- α7-Nicotinic Acetylcholine Receptor Promotes Cholangiocarcinoma Progression and Epithelial-Mesenchymal Transition Process.Digestive diseases and sciences · 2019Article
- α7 nicotinic acetylcholine receptors in lung cancer.Oncology letters · 2018Review
- Targeting EP4 downstream c-Jun through ERK1/2-mediated reduction of DNMT1 reveals novel mechanism of solamargine-inhibited growth of lung cancer cells.Journal of cellular and molecular medicine · 2017Article
- Article
- Nicotinic acetylcholine receptors and cancer.Biomedical reports · 2016Article
- Prostaglandin E2 stimulates normal bronchial epithelial cell growth through induction of c-Jun and PDK1, a kinase implicated in oncogenesis.Respiratory research · 2015Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundCyclooxygenase-2-derived prostaglandin E2 (PGE2) stimulates tumor cell growth and progression. α7 nicotinic acetylcholine receptor (nAChR) is a major mediator of cholinergic signaling in tumor cells. In the present study, we investigated the mechanisms by which PGE2 increases non-small cell lung cancer (NSCLC) proliferation via α7 nAChR induction.
methodsThe effects of PGE2 on α7 nAChR expression, promoter activity, and cell signaling pathways were detected by Western blot analysis, real time reverse transcriptase polymerase chain reaction, and transient transfection assay. The effect of PGE2 on cell growth was determined by cell viability assay.
resultsWe found that PGE2 induced α7 nAChR expression and its promoter activity in NSCLC cells. The stimulatory role of PGE2 on cell proliferation was attenuated by α7 nAChR small interfering ribonucleic acids (siRNA) or acetylcholinesterase. PGE2-induced α7 nAChR expression was blocked by an antagonist of the PGE2 receptor subtype EP4 and by EP4 siRNA. Furthermore, PGE2 enhanced α7 nAChR expression via activation of c-Jun N-terminal kinase (JNK), phosphatidylinositol 3-kinase (PI3-K), and protein kinase A (PKA) pathways followed by increased c-Jun expression, a critical transcription factor. Blockade of c-Jun diminished the effects of PGE2 on α7 nAChR promoter activity and protein expression, and cell growth.
conclusionOur results demonstrate that PGE2 promotes NSCLC cell growth through increased α7 nAChR expression. This effect is dependent on EP4-mediated activation of JNK, PI3K, and PKA signals that induce c-Jun protein expression and α7 nAChR gene promoter activity. Our findings unveil a novel link between prostanoids and cholinergic signaling.
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