| Reciprocal activation of macrophages and breast carcinoma cells by nitric oxide and colony-stimulating factor-1. | |
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MedLine Citation:
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PMID: 20876703 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Induction of inducible nitric oxide synthase (iNOS) gene expression, nitric oxide (NO) production and migration of RAW264.7 macrophages by coculture with breast cancer MDA-MB-231 cells or the addition of conditioned medium derived from MDA-MB-231 cells (MDA-CM) was identified. Increased iNOS/NO induction and migration of macrophages by MDA-CM were significantly blocked by adding the c-Jun-N-terminal protein kinase (JNK) inhibitor, SP600125, the nuclear factor-kappa B (NF-κB) inhibitor, BAY117082 and pyrrolidine dithiocarbamic acid and a dominant-negative JNK. The addition of an NO donor, Diethylenetriamine-NONOate, significantly activated expressions of MMP-9 and VEGF-A genes in breast carcinoma MDA-MD-231 cells and invasion of MDA-MB-231 cells in coculture with RAW264.7 macrophages as determined using Transwell systems, but that was inhibited by adding SP600125, BAY117082 and the nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester. Induction of heme oxygenase-1 in macrophages reduced MDA-CM-induced iNOS/NO, JNK and NF-κB activations in accordance with inhibiting VEGF-A and MMP-9 gene expressions by MDA-MB-231 cells via Transwell assays. Furthermore, VEGF, sRANKL, TNF-α, IL-1α, TGF-β, CSF-1 and MCP-1 were applied, and CSF-1 showed the most potent stimulation of iNOS/NO production and migration of macrophages. MCF-7 cells with lower CSF-1 expression than MDA-MB-231 cells showed a poor stimulatory effect on iNOS/NO production and migration of macrophages. Neutralization of CSF-1 in MDA-CM using CSF-1 antibody inhibited MDA-CM-induced iNOS protein expression and migration of macrophages, and CSF-1-induced iNOS protein and migration was blocked by adding JNK inhibitor SP and NF-κB inhibitor BAY. The reciprocal activation of breast cancer and macrophages via NO-CSF-1 is first elucidated herein. |
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Authors:
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Cheng-Wei Lin; Shing-Chuan Shen; Ching-Huai Ko; Hui-Yi Lin; Yen-Chou Chen |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-09-28 |
Journal Detail:
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Title: Carcinogenesis Volume: 31 ISSN: 1460-2180 ISO Abbreviation: Carcinogenesis Publication Date: 2010 Dec |
Date Detail:
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Created Date: 2010-12-01 Completed Date: 2011-01-06 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8008055 Medline TA: Carcinogenesis Country: England |
Other Details:
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Languages: eng Pagination: 2039-48 Citation Subset: IM |
Affiliation:
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Graduate Institute of Pharmacy, School of Pharmacy, Taipei Medical University, Taipei 110, Taiwan. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Breast Neoplasms / pathology* Cell Line, Tumor Cell Movement Female Heme Oxygenase-1 / physiology Humans Macrophage Activation* Macrophage Colony-Stimulating Factor / physiology* Matrix Metalloproteinase 9 / genetics Mice Neoplasm Invasiveness Nitric Oxide / physiology* Nitric Oxide Synthase Type II / physiology Vascular Endothelial Growth Factor A / genetics |
| Chemical | |
Reg. No./Substance:
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0/Vascular Endothelial Growth Factor A; 10102-43-9/Nitric Oxide; 81627-83-0/Macrophage Colony-Stimulating Factor; EC 1.14.13.39/Nitric Oxide Synthase Type II; EC 1.14.99.3/Heme Oxygenase-1; EC 3.4.24.35/Matrix Metalloproteinase 9 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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