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
page: 59
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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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