Korean J Intern Med.  2017 Sep;32(5):780-789. 10.3904/kjim.2016.420.

Oncogenes, mitochondrial metabolism, and quality control in differentiated thyroid cancer

Affiliations
  • 1Research Center for Endocrine and Metabolic Diseases, Chungnam National University School of Medicine, Daejeon, Korea. minhos@cnu.ac.kr
  • 2Department of Medical Science, Chungnam National University School of Medicine, Daejeon, Korea.

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.

Keyword

Thyroid neoplasms; Oncogenes; Mitochondria; Metabolism

MeSH Terms

Carcinogenesis
Cell Death
Epithelial Cells
Humans
Incidence
Metabolism*
Mitochondria
Neoplasm Metastasis
Oncogenes*
Prognosis
Quality Control*
Thyroid Gland*
Thyroid Neoplasms*
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