PHD3 Loss in Cancer Enables Metabolic Reliance on Fatty Acid Oxidation via Deactivation of ACC2
详细信息 查看全文
- 作者：Natalie J. German1 ; Haejin Yoon1 ; Rushdia Z. Yusuf2 ; 3 ; J. Patrick Murphy1 ; Lydia W.S. Finley1 ; 8 ; Gaë ; lle Laurent1 ; Wilhelm Haas1 ; F. Kyle Satterstrom1 ; Jlenia Guarnerio4 ; Elma Zaganjor1 ; Daniel Santos1 ; Pier Paolo Pandolfi4 ; Andrew H. Beck5 ; Steven P. Gygi1 ; David T. Scadden2 ; 3 ; William G. Kaelin Jr.6 ; 7 ; Marcia C. Haigis1 ; 9 ; marcia_haigis@hms.harvard.edu" class="auth_mail" title="E-mail the corresponding author
- 刊名：Molecular Cell
- 出版年：2016
- 出版时间：15 September 2016
- 年：2016
- 卷：63
- 期：6
- 页码：1006-1020
- 全文大小：3302 K
文摘
- •
Prolyl hydroxylase 3 (PHD3) hydroxylates and activates the metabolic enzyme ACC2
- •
During nutrient abundance, the PHD3/ACC2 axis represses fatty acid oxidation (FAO)
- •
PHD3 is low in AML, fueling a reliance on fats that can be targeted with FAO inhibitors
- •
Re-expressing PHD3 limits FAO via ACC2 and suppresses AML in culture and in vivo