Yi Hyon-Seung, Chang Joon Young, Kim Koon Soon, Shong Minho
Research Center for Endocrine and Metabolic Diseases, Chungnam National University School of Medicine, Daejeon, Korea.
Department of Medical Science, Chungnam National University School of Medicine, Daejeon, Korea.
Korean J Intern Med. 2017 Sep;32(5):780-789. doi: 10.3904/kjim.2016.420. Epub 2017 Aug 22.
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.
甲状腺癌是内分泌器官最常见的恶性肿瘤之一，在过去几十年中其发病率稳步上升。大多数源自甲状腺上皮细胞的分化型甲状腺肿瘤表现为生长缓慢的癌症，这些肿瘤患者通过手术切除和放射性碘治疗可获得良好预后。然而，一小部分患者患有晚期甲状腺癌，并且对目前的药物治疗方式异常耐药。甲状腺肿瘤发生是一个复杂的过程，受癌基因激活、肿瘤抑制因子失活以及程序性细胞死亡改变的调控。线粒体在甲状腺癌的肿瘤形成、进展和转移过程中起重要作用。最近的研究已成功观察到甲状腺癌发生的线粒体病因。本综述重点关注在理解与线粒体代谢改变相关的甲状腺癌分子机制方面取得的最新进展。
