The lncRNA myocardial infarction associated transcript-centric competing endogenous RNA network in non-small-cell lung cancer
Received 22 January 2018
Accepted for publication 16 March 2018
Published 14 May 2018 Volume 2018:10 Pages 1155—1162
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 3
Editor who approved publication: Dr Leylah Drusbosky
Chang Zheng,1,2 Xuelian Li,2 Biyun Qian,3 Nannan Feng,3 Sumeng Gao,3 Yuxia Zhao,4 Baosen Zhou1,2
1Department of Clinical Epidemiology and Center of Evidence-Based Medicine, The First Affiliated Hospital, China Medical University, Shenyang 110001, People’s Republic of China; 2Department of Epidemiology, School of Public Health, China Medical University, Shenyang 110122, People’s Republic of China; 3Department of Epidemiology, School of Public Health, Shanghai Jiao Tong University, Shanghai 200240, People’s Republic of China; 4Department of Radiotherapy, The Fourth Affiliated Hospital of China Medical University, Shenyang, 110032, People’s Republic of China
Background: The leading cause of death for cancer is lung cancer, of which the majority subtype is non-small cell lung cancer (NSCLC). Recent studies have shown long non-coding RNAs are transcribed and contribute to cancer. Previous study has shown that a few single nucleotide polymorphisms (SNPs) in myocardial infarction associated transcript (MIAT) were associated with some diseases or function as competing endogenous RNA (ceRNA) in some cancer.
Patients and methods: We performed bioinformatic methods for analyzing RNA-seq and miRNA-seq data of NSCLC from The Cancer Genome Atlas database. 1352 NSCLC patients and 1320 cancer-free controls for genotyping, and dual luciferase reporter assay, real-time PCR are performed in A549 and H1975 lung cancer cell lines. Results are analyzed by SPSS v16.0.
Results: In the present study, we focus on the role of over-expression MIAT in NSCLC. We confirmed that rs1061451 T>C (allele odds ratio = 0.22; P < 0.01) was associated with NSCLC. Furthermore, we constructed MIAT-centric ceRNA network, and three mRNAs (MYO1B, SGK1 and WNT9A) was identified as targets by MIAT via miR-133a-5p.
Conclusion: C-containing genotypes of MIAT rs1061451 were protective factor of NSCLC, and MIAT, which may act as ceRNA via miR-133a-5p, modulated MYO1B, SGK1 and WNT9A expression level.
Keywords: non-coding RNA, non-small-cell lung cancer, single-nucleotide polymorphism, competing endogenous RNA
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