Adipocyte culture medium stimulates production of macrophage inhibitory cytokine 1 in MDA-MB-231 cells

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Title
Adipocyte culture medium stimulates production of macrophage inhibitory cytokine 1 in MDA-MB-231 cells
Author(s)
J H Kim; K Y Kim; J H Jeon; S H Lee; J E Hwang; J H Lee; K K Kim; J S Lim; K I Kim; E Y Moon; Hee Gu Lee; J H Ryu; Y Yang
Bibliographic Citation
Cancer Letters, vol. 261, no. 2, pp. 253-262
Publication Year
2008
Abstract
Obesity is one of the potential risk factors in causing breast cancer. As a result, adipose tissue surrounding breast ductal cells may play an important role in the breast cancer development or progression. To identify the genes that are regulated by factors secreted from adipocytes in breast cancer cells, MDA-MB-231 cells were treated with the culture medium of adipocytes. Most of induced genes were related to immune function and wound healing, which share a common gene expression signature with cancer progression. In present study macrophage inhibitory cytokine 1 (MIC-1) gene was studied among the induced genes. It was found that both MIC-1 mRNA and protein were dramatically increased by the culture medium of adipocytes. Furthermore, proteinase K-treated adipocyte culture supernatants also induced MIC-1 expression. These findings indicate that proteins are not major MIC-1 inducing factors in adipocyte culture medium. Consequently, we examined the effect of free fatty acids such as palmitate and oleate on MIC-1 induction and found that palmitate markedly induced MIC-1 gene expression, whereas oleate did not. Adipocyte culture medium- and palmitate-induced MIC-1 gene expression was mediated by the activation of p38 MAPK, but not by the activation of JNK, ERK, and NF-κB pathway. In addition, adipocyte-CM-induced MIC-1 also increased invasiveness of MDA-MB-231 cells.
Keyword
AdipocytesBreast cancerMDA-MB-231MIC-1
ISSN
0304-3835
Publisher
Elsevier
DOI
http://dx.doi.org/10.1016/j.canlet.2007.11.020
Type
Article
Appears in Collections:
Division of Biomedical Research > Immunotherapy Research Center > 1. Journal Articles
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