Bisphenol A diglycidyl ether induces apoptosis in tumour cells independently of peroxisome proliferator-activated receptor-γ, in caspase-dependent and -independent manners
Bisphenol A diglycidyl ether induces apoptosis in tumour cells independently of peroxisome proliferator-activated receptor-γ, in caspase-dependent and -independent manners
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DOI：
10.1042/0264-6021:3620573
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发表时间：
2002-03-15
影响因子：
4.1
通讯作者：
Göke, R
中科院分区：
文献类型：
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作者：
Fehlberg, S;Trautwein, S;Göke, R
过氧化物酶体增殖物激活受体(PPAR)是一类核转录因子，参与调节细胞分化、脂质代谢、炎症和细胞死亡等多种生物学过程。PPAR由PPAR-α、PPAR-Delta和PPAR-Gamma三个家族组成。双酚A二缩水甘油醚(BAGE)被认为是PPAR-γ的纯拮抗剂。然而，最近的数据也揭示了BAGE的PPAR-伽马激动剂活性。在这里，我们发现BAGE通过凋亡来杀死转化的细胞，并促进肿瘤坏死因子相关的凋亡诱导配体(TRAIL)和消炎痛的细胞毒作用。BAGE的细胞毒作用不需要PPAR-γ的表达，并且是通过caspase依赖和非caspase依赖的方式介导的。
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-alpha, PPAR-delta and PPAR-gamma. Bisphenol A diglycidyl ether (BADGE) has been described as a pure antagonist of PPAR-gamma. However, recent data also revealed PPAR-gamma-agonistic activities of BADGE. Here we show that BADGE kills trans-formed 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-gamma expression and is mediated in caspase-dependent and caspase-independent manners.