ArticleCells2022
S1P-Induced TNF-α and IL-6 Release from PBMCs Exacerbates Lung Cancer-Associated Inflammation.
Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- IL-6/IL-6R-Mediated Mechanisms in Lung Cancer: From Pathogenesis to Potential Therapeutic Targets.Immunology · 2026Review
- Sphingosine-1-phosphate induces angiogenesis via the activating STAT3 signaling pathway to drive colorectal cancer progression.Journal of gastrointestinal oncology · 2026Article
- Integrated Serum Pharmacochemistry, Metabolomics, and Network Pharmacology to Reveal the Material Basis and Mechanism of Juan-tong-yin in the Treatment of Endometriosis.Applied biochemistry and biotechnology · 2026Article
- Chronic IL-21 exposure reshapes pulmonary environment, elevating risk of respiratory diseases.Cellular and molecular life sciences : CMLS · 2026Article
- Aberrant lipid metabolism reshapes the immune landscape in bone metastasis of nasopharyngeal carcinoma.Journal for immunotherapy of cancer · 2025Article
- Combined Serum IL-6 and CYFRA 21-1 as Potential Biomarkers for Radon-Associated Lung Cancer Risk: A Pilot Study.Biomedicines · 2025Article
- CDH3 promotes the progression of lung adenocarcinoma through driving epithelial-mesenchymal transition progress.Journal of translational medicine · 2025Article
- Role of the "inflammation-immunity-metabolism" network in non-small cell lung cancer: a multi-omics analysis.Discover oncology · 2025Article
- Context-Dependent Roles of Four Classes of Bioactive Lipids in Neuroglia-Mediated Regulation of Neuroinflammation.Journal of pain research · 2025Review
- Impact of asthma and/or chronic obstructive pulmonary disease on the survival of patients with lung adenocarcinoma.Therapeutic advances in medical oncology · 2025Article
- Spatiotemporal sphingosine-1-phosphate receptor 3 expression within the cerebral vasculature after ischemic stroke.iScience · 2024Article
- Signaling controversy and future therapeutical perspectives of targeting sphingolipid network in cancer immune editing and resistance to tumor necrosis factor-α immunotherapy.Cell communication and signaling : CCS · 2024Review
- Unraveling the Role of the Glycogen Synthase Kinase-3β, Bruton's Tyrosine Kinase, and Sphingosine 1 Phosphate Pathways in Multiple Sclerosis.Endocrine, metabolic & immune disorders drug targets · 2024Review
- How do sphingosine-1-phosphate affect immune cells to resolve inflammation?Frontiers in immunology · 2024Review
- The role of sphingosine-1-phosphate in autophagy and related disorders.Cell death discovery · 2023Review
- Sex Differences in Sphingosine-1-Phosphate Levels Are Dependent on Ceramide Synthase 1 and Ceramidase in Lung Physiology and Tumor Conditions.International journal of molecular sciences · 2023Article
- Induction of Inflammation Disrupts the Negative Interplay between STING and S1P Axis That Is Observed during Physiological Conditions in the Lung.International journal of molecular sciences · 2023Article
- HOXC11 drives lung adenocarcinoma progression through transcriptional regulation of SPHK1.Cell death & disease · 2023Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sphingosine-1-phosphate (S1P) is involved in inflammatory signaling/s associated with the development of respiratory disorders, including cancer. However, the underlying mechanism/s are still elusive. The aim of this study was to investigate the role of S1P on circulating blood cells obtained from healthy volunteers and non-small cell lung cancer (NSCLC) patients. To pursue our goal, peripheral blood mononuclear cells (PBMCs) were isolated and stimulated with S1P. We found that the administration of S1P did not induce healthy PBMCs to release pro-inflammatory cytokines. In sharp contrast, S1P significantly increased the levels of TNF-α and IL-6 from lung cancer-derived PBMCs. This effect was S1P receptor 3 (S1PR3)-dependent. The pharmacological blockade of ceramidase and sphingosine kinases (SPHKs), key enzymes for S1P synthesis, completely reduced the release of both TNF-α and IL-6 after S1P addition on lung cancer-derived PBMCs. Interestingly, S1P-induced IL-6, but not TNF-α, release from lung cancer-derived PBMCs was mTOR- and K-Ras-dependent, while NF-κB was not involved. These data identify S1P as a bioactive lipid mediator in a chronic inflammation-driven diseases such as NSCLC. In particular, the higher presence of S1P could orchestrate the cytokine milieu in NSCLC, highlighting S1P as a pro-tumor driver.
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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.