ArticleThe Journal of biological chemistry2011
Tumor-secreted PGE2 inhibits CCL5 production in activated macrophages through cAMP/PKA signaling pathway.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 61 citations in OpenAlex.
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- DeepFGRN: inference of gene regulatory network with regulation type based on directed graph embedding.Briefings in bioinformatics · 2024Article
- cAMP-PKA/EPAC signaling and cancer: the interplay in tumor microenvironment.Journal of hematology & oncology · 2024Review
- Role of EP4 factor in paediatric type 1 diabetes mellitus: a comprehensive review focusing on the honeymoon period.Pediatric endocrinology, diabetes, and metabolism · 2024Review
- Oxylipin metabolism is controlled by mitochondrial β-oxidation during bacterial inflammation.Nature communications · 2022Article
- Tumor Secretome to Adoptive Cellular Immunotherapy: Reduce Me Before I Make You My Partner.Frontiers in immunology · 2021Review
- Increased Epoxyeicosatrienoic Acids and Hydroxyeicosatetraenoic Acids After Treatment of Iodide Intake Adjustment and 1,25-Dihydroxy-Vitamin DFrontiers in physiology · 2021Article
- Effective Method for Accurate and Sensitive Quantitation of Rapid Changes of Newly Synthesized Proteins.Analytical chemistry · 2020Article
- Large-Scale Production of Human iPSC-Derived Macrophages for Drug Screening.International journal of molecular sciences · 2020Article
- Eicosanoids: Atherosclerosis and cardiometabolic health.Journal of clinical & translational endocrinology · 2020Review
- Macrophage migration inhibitory factor facilitates prostaglandin EJournal of neuroinflammation · 2019Article
- Genetic Variation in CCL5 Signaling Genes and Triple Negative Breast Cancer: Susceptibility and Prognosis Implications.Frontiers in oncology · 2019Article
- Identification of Caspase-6 as a New Regulator of Alternatively Activated Macrophages.The Journal of biological chemistry · 2016Article
- Indomethacin sensitizes resistant transformed cells to macrophage cytotoxicity.Immunology letters · 2016Article
- Myeloid Cell Prostaglandin E2 Receptor EP4 Modulates Cytokine Production but Not Atherogenesis in a Mouse Model of Type 1 Diabetes.PloS one · 2016Article
- Prostaglandin E2 receptor EP4 as the common target on cancer cells and macrophages to abolish angiogenesis, lymphangiogenesis, metastasis, and stem-like cell functions.Cancer science · 2014Article
- Regulation of chemokine expression in the tumor microenvironment.Critical reviews in immunology · 2014Review
- The two main forms of histiocytic sarcoma in the predisposed Flatcoated retriever dog display variation in gene expression.PloS one · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
One of the major characteristics of tumors is their ability to evade immunosurveillance through altering the properties and functions of host stromal and/or immune cells. CCL5 has been shown to play important roles in T cell proliferation, IFN-γ, and IL-2 production, which promotes the differentiation and proliferation of Th1 cells important for immune defense against intracellular infection. In this study we found that tumor-bearing mice were more susceptible to bacterial infection and showed reduced CCL5 levels in serum during endotoxic shock. Our data further demonstrated that the soluble factors secreted by mammary gland tumor cells but not normal mammary gland epithelial cells inhibited CCL5 expression in macrophages in response to LPS, but not to TNF-α stimulation. The inhibitory effect of tumor-secreted molecules on LPS-induced CCL5 expression was regulated at the post-transcriptional level. Blocking PGE(2) synthesis by NS398 or through the use of PGE(2) receptor antagonists AH-6809 (EP2 antagonist) and AH-23848 (EP4 antagonist) completely reversed the inhibitory effect of tumor-conditioned medium (TCM) on LPS-induced CCL5 expression. Moreover, PGE(2) and the cAMP analog forskolin could mimic tumor-mediated CCL5 inhibition, and the inhibitory effects of TCM, PGE(2), and cAMP analog on LPS-induced CCL5 expression could be completely reversed by the PKA inhibitor H89. Furthermore, blocking PGE(2) synthesis in vivo led to partial recovery of CCL5 production during endotoxic shock. Taken together, our data indicate that PGE(2) secreted from breast cancer cells suppresses CCL5 secretion in LPS-activated macrophages through a cAMP/PKA signaling pathway, which may result in suppression of host immune responses against subsequent bacterial infection.
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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.