MUTATIONAL ANALYSIS OF MITOCHONDRIAL tRNA GENES
IN PATIENTS WITH LUNG CANCER
He ZF, Zheng LC, Xie DY, Yu SS, Zhao J
*Corresponding Author: Dr. Jun Zhao, First Affiliated Hospital, Soochow University, Shizi Road, 215006, Suzhou, People’s
Republic of China. Tel./Fax: +86-0512-65223637. E-mail: zhaojsz001@163.com
page: 45
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INTRODUCTION
Over the last century, lung cancer from the rarest of
diseases became the biggest cancer killer of men worldwide
and in some parts of the world also of women. It is the most
common type of cancer diagnosed in the world and is the
number one cancer killer in the US [1]. Survival rates in
patients with lung cancer are much lower than patients with
other common cancers, such as breast, colon or prostate
cancer. It is estimated that by 2035, the number of lung cancer
deaths will increase globally by 86.0% when compared
to 2012 [2]. However, to date, the molecular mechanism
underlying this disease remains poorly understood.
Mitochondria are cellular organelles with distinct
features that belie their origins and unique functions. Originally
derived from ancient aerobic bacteria, mitochondria
are critical for meeting cellular energy demands by driving
the synthesis of ATP [3]. Mitochondria also influence cellular
signaling and survival pathways, including apoptosis
[4]. Mitochondrial dysfunction has been implicated in a
plethora of human diseases, most notably in cancer [5].
In addition, due to the lack of protective histones, introns
and efficient DNA repair systems, mitochondrial DNA
(mtDNA) acquires 10-fold more mutations than nuclear
genomic DNA [6]. Among these mutations, mitochondrial
tRNA (mt-tRNA) genes are hot-spots for pathological mutations
and over 200 mt-tRNA mutations have been linked to
various disease states [7,8]. Nevertheless, little is known
regarding the mt-tRNA mutations in lung cancer.
In this study, we performed a systematic and extensive
mutational screening for 22 mt-tRNA genes with lung
cancer. We also used the pathogenicity scoring system for
these mutations.
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