Alpha‐eleostearic acid suppresses proliferation of MCF‐7 breast cancer cells via activation of PPARγ and inhibition of ERK 1 / 2

Alpha‐eleostearic acid (α‐ESA) is known to suppress the growth in cancer cells although its underlying molecular mechanisms have not been fully elucidated. The present study was designed to elucidate and evaluate the anticancer mechanism of α‐ESA on MCF‐7 breast cancer cells. Also, an attempt was made to better understand the anticancer mechanism by which α‐ESA activated PPARγ and attenuated the ERK1/2 MAPK phosphorylation state. The MCF‐7 breast cancer cell‐line and nontumorigenic MCF‐10A human mammary epithelial cells were treated with α‐ESA and compared with negative control (without treatment) and positive control groups (treated with rosiglitazone), and changes of apoptosis‐related molecules, PPARγ and pERK1/2 were examined. In MCF‐7 cells treated with α‐ESA, we found that the expression of p53, p21, and Bax was up‐regulated whereas expression of Bcl‐2 and procaspase‐9 was down‐regulated. Moreover, nuclear translocation of PPARγ by α‐ESA positively correlated with inhibition of ERK1/2 activation. Our data suggest that α‐ESA can be considered to be a PPARγ agonist and thus a candidate for a chemotherapeutic agent against breast cancer. (Cancer Sci 2009; 00: 000–000)