| Soluble factors derived from tumor mammary cell lines induce a stromal mammary adipose reversion in human and mice adipose cells. Possible role of TGF-beta1 and TNF-alpha. | |
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MedLine Citation:
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PMID: 19649705 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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In carcinomas such as those of breast, pancreas, stomach, and colon, cancer cells support the expansion of molecular and cellular stroma in a phenomenon termed desmoplasia, which is characterized by a strong fibrotic response. In the case of breast tissue, in which stroma is mainly a fatty tissue, this response presumably occurs at the expense of the adipose cells, the most abundant stromal phenotype, generating a tumoral fibrous structure rich in fibroblast-like cells. In this study, we aimed to determine the cellular mechanisms by which factors present in the media conditioned by MDA-MB-231 and MCF-7 human breast cancer cell lines induce a reversion of adipose cells to a fibroblastic phenotype. We demonstrated that soluble factors generated by these cell lines stimulated the reversion of mammary adipose phenotype evaluated as intracellular lipid content and expression of C/EBP alpha and PPAR gamma. We also demonstrated that exogenous TGF-beta 1 and TNF-alpha exerts a similar function. The participation of both growth factors, components of media conditioned by tumoral mammary cells, on the expression and nuclear translocation of C/EBP alpha and PPAR gamma was tested in 3T3-L1 cells by interfering with the inhibitory effects of media with agents that block the TGF-beta 1 and TNF-alpha activity. These results allow us to postulate that TGF-beta 1 and TNF-alpha present in this media are in part responsible for this phenotypic reversion. |
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Authors:
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Javier Guerrero; Nicol?s Tobar; M?nica C?ceres; Lorena Espinoza; Paula Escobar; Javier Dotor; Patricio C Smith; Jorge Mart?nez |
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Publication Detail:
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Type: Letter; Research Support, Non-U.S. Gov't Date: 2009-08-01 |
Journal Detail:
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Title: Breast cancer research and treatment Volume: 119 ISSN: 1573-7217 ISO Abbreviation: Breast Cancer Res. Treat. Publication Date: 2010 Jan |
Date Detail:
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Created Date: 2009-12-18 Completed Date: 2010-03-10 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8111104 Medline TA: Breast Cancer Res Treat Country: Netherlands |
Other Details:
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Languages: eng Pagination: 497-508 Citation Subset: IM |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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3T3-L1 Cells Adipocytes / metabolism*, pathology Animals Blotting, Western Breast Neoplasms / metabolism*, pathology, surgery CCAAT-Enhancer-Binding Proteins / metabolism Cell Line, Tumor Cell Size Cell Transdifferentiation* Culture Media, Conditioned / metabolism Female Fibroblasts / metabolism*, pathology Humans Immunohistochemistry Mice PPAR gamma / metabolism Phenotype Recombinant Proteins / metabolism Signal Transduction Transforming Growth Factor beta1 / metabolism* Tumor Necrosis Factor-alpha / metabolism* |
| Chemical | |
Reg. No./Substance:
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0/CCAAT-Enhancer-Binding Proteins; 0/CEBPA protein, human; 0/CEBPA protein, mouse; 0/Culture Media, Conditioned; 0/PPAR gamma; 0/Recombinant Proteins; 0/Transforming Growth Factor beta1; 0/Tumor Necrosis Factor-alpha |
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