Abstract
Abstract The peroxisome proliferator-activated receptor-β/δ (PPARβ/δ) regulates a variety of biological processes but the function of PPARβ/δ in carcinogenesis remains controversial. Stable human cancer cell lines (A431, MDA-MB-231 and MCF7) that constitutively over-express PPARβ/δ were produced to effectively examine the role of this receptor in human cancer models. Ligand activation of PPARβ/δ both in MDA-MB-231 (ER-negative) and MCF7 (ER-positive) cells over-expressing PPARβ/δ cells caused significantly decreased clonogenicity compared to controls. Over-expression of PPARβ/δ reduced tumor volumes and tumor weights of ectopic xenografts from both MDA-MB-231 and MCF7cells compared to controls. Ligand activation of PPARβ/δ caused an even greater reduction of tumor volumes and tumor weights compared to controls. Interestingly, similar results were observed in the human epidermoid carcinoma cell line A431 and other human cancer cell lines. Ligand activation of PPARβ/δ strongly inhibited clonogenicity in A431 cells over-expressing PPARβ/δ. Xenografts from A431 control cells rapidly developed tumors while tumors were barely detectable in A431 cells over-expressing PPARβ/δ. These observations demonstrate the inhibitory effect of activating or over-expressing PPARβ/δ on tumorigenesis in human cancer cell lines. This suggests that PPARβ/δ suppression of tumorigenicity may be mediated through common mechanisms. Citation Format: Pei-Li Yao, Michael G. Borland, Prasad Krishnan, Bokai Zhu, Frank J. Gonzalez, Jeffrey M. Peters. Inhibition of clonogenicity and xenograft tumor growth by activation and/or over-expression of peroxisome proliferator-activated receptor-β/δ (PPARβ/δ). [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1295. doi:10.1158/1538-7445.AM2013-1295
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