ArticlePloS one2012
Autocrine prostaglandin E2 signaling promotes tumor cell survival and proliferation in childhood neuroblastoma.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 53 citations in OpenAlex.
- Analysis of differentially expressed proteins in lymph fluids related to lymphatic metastasis in a breast cancer rabbit model guided by contrast‑enhanced ultrasound.Oncology letters · 2024Article
- Targeting the myeloid microenvironment in neuroblastoma.Journal of experimental & clinical cancer research : CR · 2023Review
- Prostaglandin E2 in neuroblastoma: Targeting synthesis or signaling?Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022Review
- Article
- Characterization of the Signaling Modalities of Prostaglandin E2 Receptors EP2 and EP4 Reveals Crosstalk and a Role for Microtubules.Frontiers in immunology · 2020Article
- Inhibition of Microsomal Prostaglandin E Synthase-1 in Cancer-Associated Fibroblasts Suppresses Neuroblastoma Tumor Growth.EBioMedicine · 2018Article
- Prosurvival effect of cumulus prostaglandin G/H synthase 2/prostaglandin2 signaling on bovine blastocyst: impact on in vivo posthatching development.Biology of reproduction · 2017Article
- Odontogenic epithelial proliferation is correlated with COX-2 expression in dentigerous cyst and ameloblastoma.Experimental and therapeutic medicine · 2017Article
- Decursinol angelate inhibits PGE2-induced survival of the human leukemia HL-60 cell line via regulation of the EP2 receptor and NFκB pathway.Cancer biology & therapy · 2016Article
- Dysregulated CRTC1 activity is a novel component of PGE2 signaling that contributes to colon cancer growth.Oncogene · 2016Article
- Intracellular EP2 prostanoid receptor promotes cancer-related phenotypes in PC3 cells.Cellular and molecular life sciences : CMLS · 2015Article
- COX/mPGES-1/PGE2 pathway depicts an inflammatory-dependent high-risk neuroblastoma subset.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Prostaglandin E2 promotes MYCN non-amplified neuroblastoma cell survival via β-catenin stabilization.Journal of cellular and molecular medicine · 2015Article
- The SK-N-AS human neuroblastoma cell line develops osteolytic bone metastases with increased angiogenesis and COX-2 expression.Journal of bone oncology · 2014Article
- COX2 expression in neuroblastoma increases tumorigenicity but does not affect cell death in response to the COX2 inhibitor celecoxib.Clinical & experimental metastasis · 2014Article
- A role for TRAIL/TRAIL-R2 in radiation-induced apoptosis and radiation-induced bystander response of human neural stem cells.Apoptosis : an international journal on programmed cell death · 2014Article
- E-type prostanoid receptor 4 (EP4) in disease and therapy.Pharmacology & therapeutics · 2013Review
- Dying endothelial cells stimulate proliferation of malignant glioma cells via a caspase 3-mediated pathway.Oncology letters · 2013Article
- Antitumor activity of the selective cyclooxygenase-2 inhibitor, celecoxib, on breast cancer in Vitro and in Vivo.Cancer cell international · 2012Article
- Cancer and inflammation: an aspirin a day keeps the cancer at bay.Current biology : CB · 2012Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundProstaglandin E(2) (PGE(2)) is an important mediator in tumor-promoting inflammation. High expression of cyclooxygenase-2 (COX-2) has been detected in the embryonic childhood tumor neuroblastoma, and treatment with COX inhibitors significantly reduces tumor growth. Here, we have investigated the significance of a high COX-2 expression in neuroblastoma by analysis of PGE(2) production, the expression pattern and localization of PGE(2) receptors and intracellular signal transduction pathways activated by PGE(2). PRINCIPAL
findingsA high expression of the PGE(2) receptors, EP1, EP2, EP3 and EP4 in primary neuroblastomas, independent of biological and clinical characteristics, was detected using immunohistochemistry. In addition, mRNA and protein corresponding to each of the receptors were detected in neuroblastoma cell lines. Immunofluorescent staining revealed localization of the receptors to the cellular membrane, in the cytoplasm, and in the nuclear compartment. Neuroblastoma cells produced PGE(2) and stimulation of serum-starved neuroblastoma cells with PGE(2) increased the intracellular concentration of calcium and cyclic AMP with subsequent phosphorylation of Akt. Addition of 16,16-dimethyl PGE(2) (dmPGE(2)) increased cell viability in a time, dose- and cell line-dependent manner. Treatment of neuroblastoma cells with a COX-2 inhibitor resulted in a diminished cell growth and viability that was reversed by the addition of dmPGE(2). Similarly, PGE(2) receptor antagonists caused a decrease in neuroblastoma cell viability in a dose-dependent manner.
conclusionsThese findings demonstrate that PGE(2) acts as an autocrine and/or paracrine survival factor for neuroblastoma cells. Hence, specific targeting of PGE(2) signaling provides a novel strategy for the treatment of childhood neuroblastoma through the inhibition of important mediators of tumor-promoting inflammation.
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