Metabolic Reprogramming in Thyroid Carcinoma

被引:41
|
作者
Coelho, Raquel Guimaraes [1 ]
Fortunato, Rodrigo S. [2 ]
Carvalho, Denise P. [1 ]
机构
[1] Univ Fed Rio de Janeiro, Inst Biofis Carlos Chagas Filho, Lab Fisiol Endocrina, Rio De Janeiro, Brazil
[2] Univ Fed Rio de Janeiro, Inst Biofis Carlos Chagas Filho, Lab Radiobiol Mol, Rio De Janeiro, Brazil
来源
FRONTIERS IN ONCOLOGY | 2018年 / 8卷
关键词
glycolysis; glutaminolysis; Warburg effect; thyroid cancer; hypoxia-inducible factor; hexokinase; AMP kinase; mammalian target of rapamycin protein; PYRUVATE-KINASE M2; POSITRON-EMISSION-TOMOGRAPHY; MITOCHONDRIAL-DNA MUTATIONS; CANCER-CELL METABOLISM; NADPH OXIDASE NOX4; C-MYC; HURTHLE CELL; LACTATE-DEHYDROGENASE; ENERGY-METABOLISM; TUMOR METABOLISM;
D O I
10.3389/fonc.2018.00082
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Among all the adaptations of cancer cells, their ability to change metabolism from the oxidative to the glycolytic phenotype is a hallmark called the Warburg effect. Studies on tumor metabolism show that improved glycolysis and glutaminolysis are necessary to maintain rapid cell proliferation, tumor progression, and resistance to cell death. Thyroid neoplasms are common endocrine tumors that are more prevalent in women and elderly individuals. The incidence of thyroid cancer has increased in the Past decades, and recent findings describing the metabolic profiles of thyroid tumors have emerged. Currently, several drugs are in development or clinical trials that target the altered metabolic pathways of tumors are undergoing. We present a review of the metabolic reprogramming in cancerous thyroid tissues with a focus on the factors that promote enhanced glycolysis and the possible identification of promising metabolic targets in thyroid cancer.
引用
收藏
页数:15
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