VARIANTS IN MITOCHONDRIAL tRNA GENE MAY NOT BE ASSOCIATED WITH THYROID CARCINOMA
Lv F1,a, Qian G2,a, You W1,a, Lin H3, Wang XF3, Qiu GS2, Jiang YS2, Pang LX3, Kang YM4, Jia BF4, Xu JZ5,*, Yu Y1,*
*Corresponding Author: Dr. Jinzhong Xu, Department of Clinical Pharmacy, the Affiliated Wenling Hospital of Wenzhou Medial University, Taiping Nan Road 190, Wenling 317500, People’s Republic of China. Tel./Fax: +86-(0)576-8620-6288. E-mail: xujzwl@163.com and Dr. Yang Yu, Department of Breast Surgery, Henan Provincial People’s Hospital, Weiwu Road 7, Zhengzhou 450003, People’s Republic of China. Tel./Fax: +86-(0)371- 6558-0014. E-mail: 510790135@qq.com
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INTRODUCTION

With an incidence of 2.0%, thyroid carcinoma is the most common form of endocrine system malignancy [1,2]. Thyroid carcinomas are histologically classified as papillary thyroid carcinoma (PTC), follicular thyroid carcinoma (FTC), anaplastic thyroid carcinoma (ATC) and medullary thyroid carcinoma (MTC), accounting for approximately 80.0, 15.0, 2.0 and 4.0% of all thyroid malignancies, respectively [3]. Decreased survival in patients with oncocytic carcinomas may be due to reduced competence in iodine uptake by the tumor cells, resulting in poor response to radioiodine treatment. However, to date, the molecular mechanism underlying this disease remain largely unknown. Since Warburg proposed that cancer originated from a non neoplastic cell that adopted anaerobic metabolism as a means of survival after injury to its respiratory system [4], changes in the number, shape, and function of mitochondria have been reported in various cancers [5]. The mitochondrial genome is a closed double-stranded circular molecule consisting of 16,569 bp coding for 37 genes, including 13 polypeptides, 22 tRNAs and two rRNAs necessary for function of the respiratory chain [6]. Due to the lack of histone protection and a poor repair system, mtDNA is thought to be more susceptible than nuclear DNA to mutagen-induced damage [7]. Of these, mt-tRNA is the hot-spot for mutations in cancers as it is preferentially damaged by many carcinogens [8]. However, some of these mutations are single nucleotide polymorphisms (SNPs) and may not cause mitochondrial dysfunction, such as the mttRNAPhe C628T variant in deafness expression [9]. Distinguishing the SNPs and mutations is important, because failure to do so will inevitably lead to poor diagnosis and genetic advice. In this study, we reassess seven reported mttRNA variants: tRNAAsp G7521A, tRNAArg T10411C and T10463C, tRNALeu(CUN) A12308G, tRNAIle G4292C and C4312T, tRNAAla T5655C, in clinical manifestation of thyroid cancer. First, we carried out database searches for the allele frequencies of these variants, and then the genotype to phenotype association of these variants. Moreover, we performed the phylogenetic conservation analysis of these variants. We further utilized the bioinformatic tool to predict the ⊿G of mt-tRNAs with and without these variants. To determine the frequency of A12308G variant, we screened this variant in 300 patients with thyroid cancer and 200 controls.



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