Oncotarget

Research Papers:

Systematic identification of long non-coding RNAs with cancer-testis expression patterns in 14 cancer types

Na Qin, Cheng Wang, Qun Lu, Zijian Ma, Juncheng Dai, Hongxia Ma, Guangfu Jin, Hongbing Shen and Zhibin Hu _

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Oncotarget. 2017; 8:94769-94779. https://doi.org/10.18632/oncotarget.21930

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Abstract

Na Qin1,2,3,*, Cheng Wang1,2,3,4,*, Qun Lu2,3, Zijian Ma2,3, Juncheng Dai1,2,3, Hongxia Ma1,2,3, Guangfu Jin1,2,3, Hongbing Shen1,2,3 and Zhibin Hu1,2,3

1State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing 211166, China

2Department of Epidemiology and Biostatistics, School of Public Health, Nanjing Medical University, Nanjing 211166, China

3Jiangsu Key Lab of Cancer Biomarkers, Prevention and Treatment, Collaborative Innovation Center for Cancer Medicine, Nanjing Medical University, Nanjing 211166, China

4Department of Bioinformatics, School of Basic Medical Sciences, Nanjing Medical University, Nanjing 211116, China

*These authors have contributed equally to this work

Correspondence to:

Zhibin Hu, email: zhibin_hu@njmu.edu.cn

Keywords: cancer-testis gene; long non-coding RNA; genomic instability; lung adenocarcinoma

Received: June 28, 2017    Accepted: August 08, 2017    Published: October 19, 2017

ABSTRACT

Cancer-testis (CT) genes are a group of genes that are potential targets of immunotherapy and candidate epi-drivers participating in the development of cancers. Previous studies mainly focused on protein-coding genes, neglecting long non-coding RNAs with the same expression patterns. In this study, we performed a systematic investigation of cancer-testis long non-coding RNAs (CT-lncRNAs) with multiple independent open-access databases.We identified 1,325 extremely highly expressed CT-lncRNAs (EECT-lncRNAs) in 14 cancer types. Functional annotation revealed that CT-lncRNAs reactivated in cancers could promote genome instability and the malignant potential of cancers. We observed a mutually exclusive pattern of EECT-lncRNA activation and mutation in known oncogenes, suggesting their potential role as drivers of cancer that complement known mut-driver genes. Additionally, we provided evidence that testis-specific regulatory elements and promoter hypo-methylation may be EECT-lncRNA activation mechanisms, and EECT-lncRNAs may regulate CT gene reactivation. Taken together, our study puts forth a new hypothesis in the research field of CT genes, whereby CT-lncRNAs/EECT-lncRNAs play important roles in the progression and maintenance of tumorigenesis, expanding candidate CT epi-driver genes from coding genes to non-coding RNAs.


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