Establishing the Role of PPAR尾/未 in Carcinogenesis

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• 作者：Jeffrey M. Peters¹ ; ^{jmp21@psu.edu" class="auth_mail" title="E-mail the corresponding author} ; Frank J. Gonzalez² ; Rolf Mü ; ller³
• 关键词：peroxisome proliferator-activated receptor-尾/未 ; cancer ; chemoprevention ; mechanisms ; transcription factor
• 刊名：Trends in Endocrinology & Metabolism
• 出版年：2015
• 出版时间：November 2015
• 年：2015
• 卷：26
• 期：11
• 页码：595-607
• 全文大小：2145 K

文摘

The role of the nuclear hormone receptor peroxisome proliferator-activated receptor 尾/未 (PPAR尾/未) in carcinogenesis is controversial because conflicting studies indicate that it both inhibits and promotes tumorigenesis. In this review, we focus on recent studies on PPAR尾/未 including the significance of increased or decreased PPAR尾/未 expression in cancers; a range of opposing mechanisms describing how PPAR尾/未 agonists, antagonists, and inverse agonists regulate tumorigenesis and/or whether there may be cell context-specific mechanisms; and whether activating or inhibiting PPAR尾/未 is feasible for cancer chemoprevention and/or therapy. Research questions that need to be addressed are highlighted to establish whether PPAR尾/未 can be effectively targeted for cancer chemoprevention.