Targeting metabolic reprogramming as a potential therapeutic strategy in melanoma

被引:29
|
作者
Smith, Lorey K. [1 ,2 ]
Rao, Aparna D. [1 ,2 ]
McArthur, Grant A. [1 ,2 ,3 ,4 ,5 ]
机构
[1] Peter MacCallum Canc Ctr, Oncogen Signaling & Growth Control Program, Mol Oncol Lab, Melbourne, Vic 8006, Australia
[2] Univ Melbourne, Sir Peter MacCallum Dept Oncol, Melbourne, Vic 3010, Australia
[3] Peter MacCallum Canc Ctr, Canc Therapeut Program, Translat Res Lab, Melbourne, Vic 8006, Australia
[4] Univ Melbourne, Dept Pathol, Melbourne, Vic 3010, Australia
[5] Univ Melbourne, St Vincents Hosp, Dept Med, Melbourne, Vic 3010, Australia
关键词
BRAF(V600E); NRAS; Melanoma; Metabolism; BRAF-MUTANT MELANOMA; OXIDATIVE-PHOSPHORYLATION; GLUTAMINE-METABOLISM; MALIGNANT-MELANOMA; RAS; CANCER; RESISTANCE; MUTATIONS; GROWTH; INHIBITION;
D O I
10.1016/j.phrs.2016.02.009
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Metabolic reprogramming is a recognized hallmark of cancer. In order to support continued proliferation and growth, tumor cells must metabolically adapt to balance their bio energetic and biosynthetic needs. To achieve this, cancer cells switch from mitochondrial oxidative phosphorylation to predominantly rely on glycolysis, a process known as the "Warburg effect". The BRAF oncogene has recently emerged as a critical regulator of this process in melanoma, bringing to the fore the importance of metabolic reprogramming in the pathogenesis and treatment of metastatic melanoma. In this review, we summarize our current understanding of oncogenic reprogramming of metabolism in BRAF and NRAS mutant melanoma, and highlight emerging evidence supporting a metabolic basis for MAPK pathway inhibitor resistance and metabolic vulnerabilities that may be exploited to overcome this. (C) 2016 Elsevier Ltd. All rights reserved.
引用
收藏
页码:42 / 47
页数:6
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