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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Abstract
Thyroid cancer is a very common form of endocrine
system malignancy. To date, the molecular
mechanism underlying thyroid cancer remains poorly
understood. Studies of oncocytic tumors have led to
a hypothesis which proposes that defects in oxidative
phosphorylation (OX- PHOS) may result in a
compensatory increase in mitochondrial replication
and gene expression. As a result, mitochondrial DNA
(mtDNA) mutation analysis has become a useful tool
to explore the molecular basis of this disease. Among
these mutations, mitochondrial transfer RNAs (mttRNAs)
are the hot spots for pathogenic mutations associated
with thyroid cancer. However, due to its high
mutation rate, the role of mt-tRNA variants in thyroid
cancer is still controversial. To address this problem,
in this study, we reassessed seven reported mt-tRNA
variants: tRNAAsp G7521A, tRNAArg T10411C and
T10463C, tRNALeu(CUN) A12308G, tRNAIle G4292C
and C4312T, and tRNAAla T5655C, in clinical manifestations
of thyroid cancer. We first performed the
phylogenetic conservation analysis for these variants;
moreover, we used a bioinformatic tool to compare
the minimum free energy (G) of mt-tRNA with and
without mutations. Most strikingly, none of these
variants caused the significant change of the G between
the wild-type and the mutant form, suggesting
that they may not play an important roles in thyroid
cancer. In addition, we screened the frequency of the
“pathogenic” A12308G alternation in 300 patients
with thyroid cancer and 200 healthy controls. We
found that there were five patients and three control
subjects carrying this variant. It seemed that the
A12308G variant may be a common polymorphism
in the human population. Taken together, our study
indicated that variants in mt-tRNA genes may not
play active roles in patients with thyroid cancer.
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