Metabolic Alterations of Thyroid Cancer as Potential Therapeutic Targets

被引:36
作者
Ciavardelli, Domenico [1 ,2 ]
Bellomo, Maria [1 ]
Consalvo, Ada [2 ]
Crescimanno, Caterina [1 ]
Vella, Veronica [1 ,3 ]
机构
[1] Univ Kore Enna, Sch Human & Social Sci, Enna, Italy
[2] Ctr Sci Invecchiamento & Med Traslaz CeSI Met, Chieti, Italy
[3] Univ Catania, Garibaldi Nesima Hosp, Endocrinol Sect, Dept Clin & Expt Med, Catania, Italy
关键词
POSITRON-EMISSION-TOMOGRAPHY; GLUT1; GLUCOSE-TRANSPORTER; PYRUVATE-KINASE M2; BRAF MUTATION; LACTATE METABOLISM; EXPRESSION; TUMOR; CARCINOMA; DIAGNOSIS; RECEPTOR;
D O I
10.1155/2017/2545031
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
Thyroid cancer (TC) is the most frequent endocrine tumor with a growing incidence worldwide. Besides the improvement of diagnosis, TC increasing incidence is probably due to environmental factors and lifestyle modifications. The actual diagnostic criteria for TC classification are based on fine needle biopsy (FNAB) and histological examination following thyroidectomy. Since in some cases it is not possible to make a proper diagnosis, classical approach needs to be supported by additional biomarkers. Recently, new emphasis has been given to the altered cellular metabolism of proliferating cancer cells which require high amount of glucose for energy production and macromolecules biosynthesis. Also TC displays alteration of energy metabolism orchestrated by oncogenes activation and tumor suppressors inactivation leading to abnormal proliferation. Furthermore, TC shows significant metabolic heterogeneity within the tumor microenvironment and metabolic coupling between cancer and stromal cells. In this review we focus on the current knowledge of metabolic alterations of TC and speculate that targeting TC metabolism may improve current therapeutic protocols for poorly differentiated TC. Future studies will further deepen the actual understandings of the metabolic phenotype of TC cells and will give the chance to provide novel prognostic biomarkers and therapeutic targets in tumors with a more aggressive behavior.
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页数:10
相关论文
共 97 条
[1]   The Bethesda System for Reporting Thyroid Cytopathology II [J].
Ali, Syed Z. ;
Cibas, Edmund S. .
ACTA CYTOLOGICA, 2016, 60 (05) :397-+
[2]   Serine and glycine metabolism in cancer [J].
Amelio, Ivano ;
Cutruzzola, Francesca ;
Antonov, Alexey ;
Agostini, Massimiliano ;
Melino, Gerry .
TRENDS IN BIOCHEMICAL SCIENCES, 2014, 39 (04) :191-198
[3]   Incidence and clinical characteristics of thyroid carcinoma after iodine prophylaxis in an endemic goiter country [J].
BacherStier, C ;
Riccabona, G ;
Totsch, M ;
Kemmler, G ;
Oberaigner, W ;
Moncayo, R .
THYROID, 1997, 7 (05) :733-741
[4]   Metabolic Regulation by p53 Family Members [J].
Berkers, Celia R. ;
Maddocks, Oliver D. K. ;
Cheung, Eric C. ;
Mor, Inbal ;
Vousden, Karen H. .
CELL METABOLISM, 2013, 18 (05) :617-633
[5]   Rapid accumulation of Akt in mitochondria following phosphatidylinositol 3-kinase activation [J].
Bijur, GN ;
Jope, RS .
JOURNAL OF NEUROCHEMISTRY, 2003, 87 (06) :1427-1435
[6]   Glucose-deprivation increases thyroid cancer cells sensitivity to metformin [J].
Bikas, Athanasios ;
Jensen, Kirk ;
Patel, Aneeta ;
Costello, John, Jr. ;
McDaniel, Dennis ;
Klubo-Gwiezdzinska, Joanna ;
Larin, Olexander ;
Hoperia, Victoria ;
Burman, Kenneth D. ;
Boyle, Lisa ;
Wartofsky, Leonard ;
Vasko, Vasyl .
ENDOCRINE-RELATED CANCER, 2015, 22 (06) :919-932
[7]  
Bläser D, 2006, J NUCL MED, V47, P1382
[8]   Metabolic pathways promoting cancer cell survival and growth [J].
Boroughs, Lindsey K. ;
DeBerardinis, Ralph J. .
NATURE CELL BIOLOGY, 2015, 17 (04) :351-359
[9]   Expression of hypoxia-inducible factor 1α in thyroid carcinomas [J].
Burrows, N. ;
Resch, J. ;
Cowen, R. L. ;
von Wasielewski, R. ;
Hoang-Vu, C. ;
West, C. M. ;
Williams, K. J. ;
Brabant, G. .
ENDOCRINE-RELATED CANCER, 2010, 17 (01) :61-72
[10]   Hypoxia-Inducible Factor in Thyroid Carcinoma [J].
Burrows, Natalie ;
Babur, Muhammad ;
Resch, Julia ;
Williams, Kaye J. ;
Brabant, Georg .
JOURNAL OF THYROID RESEARCH, 2011, 2011