Spotlight on GOT2 in Cancer Metabolism

被引:7
|
作者
Kerk, Samuel A. [1 ]
Garcia-Bermudez, Javier [2 ]
Birsoy, Kivanc [3 ]
Sherman, Mara H. [4 ]
Shah, Yatrik M. [5 ]
Lyssiotis, Costas A. [5 ]
机构
[1] Univ Michigan, Doctoral Program Canc Biol, Ann Arbor, MI USA
[2] Univ Texas Southwestern Med Ctr, Res Inst, Childrens Med Ctr, Dallas, TX USA
[3] Rockefeller Univ, Lab Metab Regulat & Genet, New York, NY USA
[4] Mem Sloan Kettering Canc Ctr, Canc Biol & Genet Program, New York, NY USA
[5] Univ Michigan, Dept Mol & Integrat Physiol, Ann Arbor, MI 48109 USA
来源
ONCOTARGETS AND THERAPY | 2023年 / 16卷
关键词
transaminase; mitochondria; tumor microenvironment; nucleotides; redox; pancreatic cancer; FATTY-ACID TRANSPORTERS; CELL-PROLIFERATION; SHUTTLE ACTIVITY; OXIDATION; RAT; FAT/CD36; ACETYLATION; INHIBITION; EXPRESSION; INCREASES;
D O I
10.2147/OTT.S382161
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
GOT2 is at the nexus of several critical metabolic pathways in homeostatic cellular and dysregulated cancer metabolism. Despite this, recent work has emphasized the remarkable plasticity of cancer cells to employ compensatory pathways when GOT2 is inhibited. Here, we review the metabolic roles of GOT2, highlighting findings in both normal and cancer cells. We emphasize how cancer cells repurpose cell intrinsic metabolism and their flexibility when GOT2 is inhibited. We close by using this framework to discuss key considerations for future investigations into cancer metabolism.
引用
收藏
页码:695 / 702
页数:8
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