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

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.

Keywords: Metabolism; Mitochondria; Oncogenes; Thyroid neoplasms.

Figure 1.

Scientific interest in thyroid cancer from the 1950s to the present. Articles were identified in PubMed using the term “thyroid cancer” for each year from 1950 to 2014, and are expressed as the total number of thyroid cancer articles, and thyroid cancer articles as a percentage of all articles. Important milestones in the field of thyroid cancer research are indicated by the year of publication. PTC, papillary thyroid cancer; BRAF, B-Raf; NTRK1, neurotrophic receptor tyrosine kinase 1.

Figure 2.

Total number and percentage of (A) BRAF, (B) RET/PTC, (C) TRK, and (D) thyroid cancer and mitochondria articles in PubMed. BRAF, B-Raf; PTC, papillary thyroid cancer; TRK, tropomyosin receptor kinase.