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dc.contributor.author
Krasnapolski, Martin Alejandro
dc.contributor.author
Lodillinsky, Catalina
dc.contributor.author
Bal, Elisa Dora
dc.contributor.author
Eijan, Ana Maria
dc.date.available
2018-03-14T22:26:29Z
dc.date.issued
2015-10
dc.identifier.citation
Krasnapolski, Martin Alejandro; Lodillinsky, Catalina; Bal, Elisa Dora; Eijan, Ana Maria; Hypoxia-induced nitric oxide release by luminal cells stimulates proliferation and uPA secretion of myoepithelial cells in a bicellular murine mammary tumor; Springer Heidelberg; Journal Of Cancer Research And Clinical Oncology; 141; 10; 10-2015; 1727-1738
dc.identifier.issn
0171-5216
dc.identifier.uri
http://hdl.handle.net/11336/38864
dc.description.abstract
Introduction: LM38 murine mammary adenocarcinoma model is formed by LM38-LP (myoepithelial and luminal), LM38-HP (luminal) and LM38-D2 (myoepithelial) cell lines. In a previous work, we had shown that LM38-HP and LM38-D2 cell lines are less malignant than the bicellular LM38-LP cell line.
Purpose: To study the role of nitric oxide (NO) as one of the mediators of functional interactions between malignant luminal and myoepithelial cells.
Methods and results: Using immunohistochemistry, in vivo iNOS expression was only detected in the luminal cells of bicellular LM38-LP and most cells of LM38-HP tumors. In cobalt-induced pseudohypoxia, LM38-LP and LM38-HP cell lines significantly increased HIF-1α and iNOS expression (Western blotting) and therefore NO production (Griess method). This increase was inhibited by the iNOS inhibitor 1400 W. On the other side, NO was not detectable in LM38-D2 cells either in basal or in pseudohypoxia. In addition, pseudohypoxia increased urokinase-type plasminogen activator (uPA) secretion by LM38-LP and LM38-HP cells and migration in the LM38-LP cell line, without modulating these properties in LM38-D2 cells (radial caseinolysis). The NO donor DETA/NONOate (500 μM) was able to increase uPA secretion and in vitro growth of LM38-D2. In agreement, 1400 W prevented in vivo growth of the myoepithelial LM38-D2 cells.
Conclusions: Hypoxia leads to an enhanced NO production by the luminal component, through HIF-1α and iNOS, which can stimulate myoepithelial cell proliferation and uPA secretion. In these new conditions, myoepithelial cells might act as an invasive forefront generating gaps that could help luminal cells to escape from the primary tumor.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Springer Heidelberg
dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Breast Cancer
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Myoepithelial Cells
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Hypoxia
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Nitric Oxide
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Luminal Cells
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Migration
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Otras Medicina Básica
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Medicina Básica
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CIENCIAS MÉDICAS Y DE LA SALUD
dc.title
Hypoxia-induced nitric oxide release by luminal cells stimulates proliferation and uPA secretion of myoepithelial cells in a bicellular murine mammary tumor
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2018-03-13T13:58:29Z
dc.identifier.eissn
1432-1335
dc.journal.volume
141
dc.journal.number
10
dc.journal.pagination
1727-1738
dc.journal.pais
Alemania
dc.journal.ciudad
Heidelberg
dc.description.fil
Fil: Krasnapolski, Martin Alejandro. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología ; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
dc.description.fil
Fil: Lodillinsky, Catalina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología ; Argentina. Institut Curie Research Center; Francia
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Fil: Bal, Elisa Dora. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología ; Argentina
dc.description.fil
Fil: Eijan, Ana Maria. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología ; Argentina
dc.journal.title
Journal Of Cancer Research And Clinical Oncology
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1007/s00432-015-1934-1
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007%2Fs00432-015-1934-1
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