Tumour-derived and host-derived nitric oxide differentially regulate breast carcinoma metastasis to the lungs.
Identifieur interne : 002F04 ( Main/Exploration ); précédent : 002F03; suivant : 002F05Tumour-derived and host-derived nitric oxide differentially regulate breast carcinoma metastasis to the lungs.
Auteurs : RBID : pubmed:15059928English descriptors
- KwdEn :
- Animals, Cell Adhesion, Cell Division, Cell Survival, Endothelial Cells (metabolism), Endothelial Cells (pathology), Enzyme Inhibitors (pharmacology), Female, Guanidines (pharmacology), Indium Radioisotopes, Interleukin-1 (pharmacology), Lung Neoplasms (enzymology), Lung Neoplasms (secondary), Mammary Neoplasms, Experimental (enzymology), Mammary Neoplasms, Experimental (pathology), Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Knockout, Nitric Oxide (physiology), Nitric Oxide Synthase (antagonists & inhibitors), Nitric Oxide Synthase (metabolism), Nitric Oxide Synthase Type II, Survival Rate, Tumor Cells, Cultured.
- MESH :
- chemical , antagonists & inhibitors : Nitric Oxide Synthase.
- chemical , metabolism : Nitric Oxide Synthase.
- chemical , pharmacology : Enzyme Inhibitors, Guanidines, Interleukin-1.
- enzymology : Lung Neoplasms, Mammary Neoplasms, Experimental.
- metabolism : Endothelial Cells.
- pathology : Endothelial Cells, Mammary Neoplasms, Experimental.
- chemical , physiology : Nitric Oxide.
- secondary : Lung Neoplasms.
- Animals, Cell Adhesion, Cell Division, Cell Survival, Female, Indium Radioisotopes, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Knockout, Nitric Oxide Synthase Type II, Survival Rate, Tumor Cells, Cultured.
Abstract
To study the role of nitric oxide (NO) in lung metastasis of breast carcinoma, we isolated two cell clones (H and J) from the parental EMT-6 murine breast carcinoma cell line, based on their differential NO production. In vitro, EMT-6 J cells, but not EMT-6H cells, constitutively expressed inducible NO synthase (NOS II) and secreted high levels of NO. IL-1beta increased NO production in both clones, and TNF-alpha had a synergistic effect on IL-1beta-induced NO production, but NO production by EMT-6 J cells was always higher than by EMT-6H cells. Proliferation, survival and adhesion to lung-derived endothelial cells of both clones were similar and were not affected by NO. In vivo, both clones similarly located in the lungs of syngeneic mice 48 h after injection. However, EMT-6H cells were significantly more tumorigenic than EMT-6 J cells as assessed at later time points. Injection of EMT-6 J cells and simultaneous treatment of mice with aminoguanidine (AG), a NOS II inhibitor, significantly increased tumour formation. Injection of EMT-6H and EMT-6 J cells into NOS II-deficient mice resulted in a significant survival increase as compared with wild-type animals. Simultaneous administration of AG increased the death rate of NOS II-deficient mice injected with EMT-6 J cells. These results demonstrate that: (i) NO does not influence the early stages of tumour metastasis to the lungs and (ii) NOS II expression in tumour cells reduces, while NOS II expression in host cells enhances, tumour nodule development. In conclusion, the cellular origin and the local NO production are critical in the metastatic process.
DOI: 10.1093/carcin/bgh158
PubMed: 15059928
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Tumour-derived and host-derived nitric oxide differentially regulate breast carcinoma metastasis to the lungs.</title><author><name sortKey="Gauthier, Nolwenn" uniqKey="Gauthier N">Nolwenn Gauthier</name><affiliation wicri:level="1"><nlm:affiliation>EPHE/INSERM/Laboratoire d'immunologie et immunothérapie des cancers, Unité 517 et IFR 100, Université de Bourgogne, Dijon, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>EPHE/INSERM/Laboratoire d'immunologie et immunothérapie des cancers, Unité 517 et IFR 100, Université de Bourgogne, Dijon</wicri:regionArea><placeName><region type="région">Bourgogne</region><settlement type="city">Dijon</settlement></placeName></affiliation></author><author><name sortKey="Lohm, Sylvia" uniqKey="Lohm S">Sylvia Lohm</name></author><author><name sortKey="Touzery, Claude" uniqKey="Touzery C">Claude Touzery</name></author><author><name sortKey="Chantome, Aurelie" uniqKey="Chantome A">Aurélie Chantôme</name></author><author><name sortKey="Perette, Bernard" uniqKey="Perette B">Bernard Perette</name></author><author><name sortKey="Reveneau, Sylvie" uniqKey="Reveneau S">Sylvie Reveneau</name></author><author><name sortKey="Brunotte, Francois" uniqKey="Brunotte F">François Brunotte</name></author><author><name sortKey="Juillerat Jeanneret, Lucienne" uniqKey="Juillerat Jeanneret L">Lucienne Juillerat-Jeanneret</name></author><author><name sortKey="Jeannin, Jean Francois" uniqKey="Jeannin J">Jean-François Jeannin</name></author></titleStmt><publicationStmt><date when="2004">2004</date><idno type="RBID">pubmed:15059928</idno><idno type="pmid">15059928</idno><idno type="doi">10.1093/carcin/bgh158</idno><idno type="wicri:Area/Main/Corpus">003244</idno><idno type="wicri:Area/Main/Curation">003244</idno><idno type="wicri:Area/Main/Exploration">002F04</idno></publicationStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Cell Adhesion</term><term>Cell Division</term><term>Cell Survival</term><term>Endothelial Cells (metabolism)</term><term>Endothelial Cells (pathology)</term><term>Enzyme Inhibitors (pharmacology)</term><term>Female</term><term>Guanidines (pharmacology)</term><term>Indium Radioisotopes</term><term>Interleukin-1 (pharmacology)</term><term>Lung Neoplasms (enzymology)</term><term>Lung Neoplasms (secondary)</term><term>Mammary Neoplasms, Experimental (enzymology)</term><term>Mammary Neoplasms, Experimental (pathology)</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term><term>Nitric Oxide (physiology)</term><term>Nitric Oxide Synthase (antagonists & inhibitors)</term><term>Nitric Oxide Synthase (metabolism)</term><term>Nitric Oxide Synthase Type II</term><term>Survival Rate</term><term>Tumor Cells, Cultured</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Nitric Oxide Synthase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Nitric Oxide Synthase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Enzyme Inhibitors</term><term>Guanidines</term><term>Interleukin-1</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Lung Neoplasms</term><term>Mammary Neoplasms, Experimental</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Endothelial Cells</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Endothelial Cells</term><term>Mammary Neoplasms, Experimental</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Nitric Oxide</term></keywords><keywords scheme="MESH" qualifier="secondary" xml:lang="en"><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Adhesion</term><term>Cell Division</term><term>Cell Survival</term><term>Female</term><term>Indium Radioisotopes</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term><term>Nitric Oxide Synthase Type II</term><term>Survival Rate</term><term>Tumor Cells, Cultured</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">To study the role of nitric oxide (NO) in lung metastasis of breast carcinoma, we isolated two cell clones (H and J) from the parental EMT-6 murine breast carcinoma cell line, based on their differential NO production. In vitro, EMT-6 J cells, but not EMT-6H cells, constitutively expressed inducible NO synthase (NOS II) and secreted high levels of NO. IL-1beta increased NO production in both clones, and TNF-alpha had a synergistic effect on IL-1beta-induced NO production, but NO production by EMT-6 J cells was always higher than by EMT-6H cells. Proliferation, survival and adhesion to lung-derived endothelial cells of both clones were similar and were not affected by NO. In vivo, both clones similarly located in the lungs of syngeneic mice 48 h after injection. However, EMT-6H cells were significantly more tumorigenic than EMT-6 J cells as assessed at later time points. Injection of EMT-6 J cells and simultaneous treatment of mice with aminoguanidine (AG), a NOS II inhibitor, significantly increased tumour formation. Injection of EMT-6H and EMT-6 J cells into NOS II-deficient mice resulted in a significant survival increase as compared with wild-type animals. Simultaneous administration of AG increased the death rate of NOS II-deficient mice injected with EMT-6 J cells. These results demonstrate that: (i) NO does not influence the early stages of tumour metastasis to the lungs and (ii) NOS II expression in tumour cells reduces, while NOS II expression in host cells enhances, tumour nodule development. In conclusion, the cellular origin and the local NO production are critical in the metastatic process.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">15059928</PMID><DateCreated><Year>2004</Year><Month>08</Month><Day>17</Day></DateCreated><DateCompleted><Year>2004</Year><Month>10</Month><Day>05</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0143-3334</ISSN><JournalIssue CitedMedium="Print"><Volume>25</Volume><Issue>9</Issue><PubDate><Year>2004</Year><Month>Sep</Month></PubDate></JournalIssue><Title>Carcinogenesis</Title><ISOAbbreviation>Carcinogenesis</ISOAbbreviation></Journal><ArticleTitle>Tumour-derived and host-derived nitric oxide differentially regulate breast carcinoma metastasis to the lungs.</ArticleTitle><Pagination><MedlinePgn>1559-65</MedlinePgn></Pagination><Abstract><AbstractText>To study the role of nitric oxide (NO) in lung metastasis of breast carcinoma, we isolated two cell clones (H and J) from the parental EMT-6 murine breast carcinoma cell line, based on their differential NO production. In vitro, EMT-6 J cells, but not EMT-6H cells, constitutively expressed inducible NO synthase (NOS II) and secreted high levels of NO. IL-1beta increased NO production in both clones, and TNF-alpha had a synergistic effect on IL-1beta-induced NO production, but NO production by EMT-6 J cells was always higher than by EMT-6H cells. Proliferation, survival and adhesion to lung-derived endothelial cells of both clones were similar and were not affected by NO. In vivo, both clones similarly located in the lungs of syngeneic mice 48 h after injection. However, EMT-6H cells were significantly more tumorigenic than EMT-6 J cells as assessed at later time points. Injection of EMT-6 J cells and simultaneous treatment of mice with aminoguanidine (AG), a NOS II inhibitor, significantly increased tumour formation. Injection of EMT-6H and EMT-6 J cells into NOS II-deficient mice resulted in a significant survival increase as compared with wild-type animals. Simultaneous administration of AG increased the death rate of NOS II-deficient mice injected with EMT-6 J cells. These results demonstrate that: (i) NO does not influence the early stages of tumour metastasis to the lungs and (ii) NOS II expression in tumour cells reduces, while NOS II expression in host cells enhances, tumour nodule development. 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