Peroxisome proliferator-activated receptors (PPARs) are nuclear transcription factors which are involved in many biological processes, such as regulation of cell differentiation, lipid metabolism, inflammation and cell death. PPARs consist of three families, PPAR-α, PPAR-δ and PPAR-γ. Bisphenol A diglycidyl ether (BADGE) has been described as a pure antagonist of PPAR-γ. However, recent data also revealed PPAR-γ-agonistic activities of BADGE. Here we show that BADGE kills transformed cells by apoptosis and promotes the cytotoxic effects of tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) and indomethacin. The cytotoxic effect of BADGE does not require PPAR-γ expression and is mediated in caspase-dependent and caspase-independent manners.

Abbreviations used: BADGE, bisphenol A diglycidyl ether; PPAR, peroxisome proliferator-activated receptor; TRAIL, tumour necrosis factor-related apoptosis-inducing ligand; JC-1, 5,5′,6,6′-tetrachloro-1,1′,3,3′-tetraethylbenzimidazolcarbocyanine iodide; PI, propidium iodide; RT-PCR, reverse transcriptase PCR; Z-VAD-fmk, N-Benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone; Z-LEHD-fmk, N-benzyloxycarbonyl-Leu-Glu-His-Asp-fluoromethylketone.

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