Document Detail

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.
MedLine Citation:
PMID:  19649705     Owner:  NLM     Status:  MEDLINE    
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.
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:
Type:  Letter; Research Support, Non-U.S. Gov't     Date:  2009-08-01
Journal Detail:
Title:  Breast cancer research and treatment     Volume:  119     ISSN:  1573-7217     ISO Abbreviation:  Breast Cancer Res. Treat.     Publication Date:  2010 Jan 
Date Detail:
Created Date:  2009-12-18     Completed Date:  2010-03-10     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8111104     Medline TA:  Breast Cancer Res Treat     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  497-508     Citation Subset:  IM    
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MeSH Terms
3T3-L1 Cells
Adipocytes / metabolism*,  pathology
Blotting, Western
Breast Neoplasms / metabolism*,  pathology,  surgery
CCAAT-Enhancer-Binding Proteins / metabolism
Cell Line, Tumor
Cell Size
Cell Transdifferentiation*
Culture Media, Conditioned / metabolism
Fibroblasts / metabolism*,  pathology
PPAR gamma / metabolism
Recombinant Proteins / metabolism
Signal Transduction
Transforming Growth Factor beta1 / metabolism*
Tumor Necrosis Factor-alpha / metabolism*
Reg. No./Substance:
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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