Abstract

Peroxisome proliferator-activated receptor β (PPARβ) is a member of the nuclear hormone receptor superfamily and is a ligand activated transcription factor, although the precise genes that it regulates and its physiological and pathophysiological role remain unclear. In view of the association of PPARβ with colon cancer and increased mRNA levels of PPARβ in colon tumours we sought in this study to examine the expression of PPARβ in human breast epithelial cells of tumorigenic (MCF-7 and MDA-MB-231) and non-tumorigenic origin (MCF-10A). Using quantitative RT-PCR we measured PPARβ mRNA levels in MCF-7, MDA-MB-231 and MCF-10A cells at various stages in culture. After serum-deprivation, MDA-MB-231 and MCF-10A cells had a 4.2- and 3.8-fold statistically greater expression of PPARβ compared with MCF-7 cells. The tumorigenic cell lines also exhibited a significantly greater level of PPARβ mRNA after serum deprivation compared with subconfluence whereas such an effect was not observed in non-tumorigenic MCF-10A cells. The expression of PPARβ was inducible upon exposure to the PPARβ ligand bezafibrate. Our results suggest that unlike colon cancer, PPARβ overexpression is not an inherent property of breast cancer cell lines. However, the dynamic changes in PPARβ mRNA expression and the ability of PPARβ in the MCF-7 cells to respond to ligand indicates that PPARβ may play a role in mammary gland carcinogenesis through activation of downstream genes via endogenous fatty acid ligands or exogenous agonists.

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