Knockdown of Thymidine Kinase 1 Suppresses Cell Proliferation, Invasion, Migration, and Epithelial–Mesenchymal Transition in Thyroid Carcinoma Cells

Frontiers in Oncology

Chang Liu¹  Pan Zhao²  Zheng Peng²  Feiyuan Liu²  Weiqing Wu³  Li Zhao³  Hui He³  Juan Chen⁴  Jian Wang⁵  Guangsuo Wang⁵  Fajin Dong⁶ 

[1] Central Lab, Dalian Municipal Central Hospital, Dalian, China;Clinical Medical Research Center, First Affiliated Hospital of Southern University of Science and Technology, Second Clinical College of Jinan University, Shenzhen, China;Department of Health Management, First Affiliated Hospital of Southern University of Science and Technology, Second Clinical College of Jinan University, Shenzhen, China;Department of Medical Research, Shenzhen Shekou People's Hospital, Shenzhen, China;Department of Thoracic Surgery, First Affiliated Hospital of Southern University of Science and Technology, Second Clinical College of Jinan University, Shenzhen, China;Department of Ultrasound, First Affiliated Hospital of Southern University of Science and Technology, Second Clinical College of Jinan University, Shenzhen, China;

关键词: thyroid carcinoma;    thymidine kinase 1;    thyroid nodules;    progression;    miR-34a-5p;   

DOI  :  10.3389/fonc.2019.01475

来源: DOAJ

【 摘 要 】

Patients with advanced thyroid carcinoma have poor prognosis with low overall survival. Unfortunately, the underlying mechanisms of thyroid carcinoma progression remain unclear. The elevated expression of thymidine kinase 1 (TK1) has been implicated in the progression of thyroid carcinoma, while the role of TK1 in thyroid carcinoma progression has not been explored. The present study aimed to determine the role TK1 in the progression of thyroid cancer and to explore the underlying molecular mechanisms. In this study, it was found that serum TK1 levels were markedly increased in the patients with thyroid nodules. Further online data mining showed that TK1 expression was upregulated in thyroid carcinoma tissues, and higher expression of TK1 was correlated with shorter disease-free survival of patients with thyroid carcinoma. Silencing of TK1 suppressed cell proliferation, invasion, migration, and epithelial–mesenchymal transition, and also induced cell apoptosis in the thyroid carcinoma cell lines. Animal studies showed that TK1 knockdown inhibited in vivo tumor growth of thyroid carcinoma cells. Importantly, miR-34a-5p was found to be downregulated in the thyroid carcinoma cells. Furthermore, miR-34a-5p targeted the 3′ untranslated region of TK1 and suppressed the expression of TK1 in thyroid carcinoma cell lines. In summary, first, these results demonstrated the upregulation of TK1 in thyroid nodules and thyroid carcinoma tissues; second, TK1 promoted thyroid carcinoma cell proliferation, invasion, and migration; lastly, TK1 was negatively regulated by miR-34a-5p. Our study may provide novel insights into the role of TK1 in regulating thyroid carcinoma progression.

【 授权许可】

Unknown