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

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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