Oncogenes, mitochondrial metabolism, and quality control in differentiated thyroid cancer.
- Author:
Hyon Seung YI
1
;
Joon Young CHANG
;
Koon Soon KIM
;
Minho SHONG
Author Information
- Publication Type:Review
- Keywords: Thyroid neoplasms; Oncogenes; Mitochondria; Metabolism
- MeSH: Carcinogenesis; Cell Death; Epithelial Cells; Humans; Incidence; Metabolism*; Mitochondria; Neoplasm Metastasis; Oncogenes*; Prognosis; Quality Control*; Thyroid Gland*; Thyroid Neoplasms*
- From:The Korean Journal of Internal Medicine 2017;32(5):780-789
- CountryRepublic of Korea
- Language:English
- Abstract: Thyroid cancer is one of the most common malignancies of endocrine organs, and its incidence rate has increased steadily over the past several decades. Most differentiated thyroid tumors derived from thyroid epithelial cells exhibit slow-growing cancers, and patients with these tumors can achieve a good prognosis with surgical removal and radioiodine treatment. However, a small proportion of patients present with advanced thyroid cancer and are unusually resistant to current drug treatment modalities. Thyroid tumorigenesis is a complex process that is regulated by the activation of oncogenes, inactivation of tumor suppressors, and alterations in programmed cell death. Mitochondria play an essential role during tumor formation, progression, and metastasis of thyroid cancer. Recent studies have successfully observed the mitochondrial etiology of thyroid carcinogenesis. This review focuses on the recent progress in understanding the molecular mechanisms of thyroid cancer relating to altered mitochondrial metabolism.
