Adipocytes, PAI‐1 and MCF‐10A cell motility

Abstract

In addition to its role as energy stores, adipose tissue has been identified as an endocrine organ in recent years. Our understanding of the role of adipose in breast cancer development is limited, though obesity is an identified risk factor. In this study, we investigated the expression of plasminogen activator inhibitor type‐1 (PAI‐1) and urokinase plasminogen activator (uPA) in cells isolated from both omental and breast adipose tissues. uPA was not expressed in cells from either fat depot. In omental cells, PAI‐1 was more highly expressed in the preadipocytes. In cells from the breast, PAI‐1 was only expressed in the adipocytes. These results are of interest because expression of PAI‐1 is linked to poor patient survival in breast cancer. We also studied the role of breast adipocytes in breast epithelial motility, as we have seen an increase in phospho‐AKT in these cells when treated with breast adipocyte CM. We treated normal MCF‐10A cells with conditioned media (CM) from breast adipocytes and preadipocytes. Using the modified‐Boyden chamber model, we see a 2‐fold increase in MCF‐10A motility when treated with adipocyte CM, compared to preadipocyte CM. We hypothesize factors secreted from breast adipocytes, possibly PAI‐1, are inducing a more motile phenotype in the cells; further studies are needed to delineate the mechanism. These data provide a potential link between obesity and breast cancer development.