Identification of KEY lncRNAs and mRNAs Associated with Oral Squamous Cell Carcinoma Progression

Author:

Li Ju1,Zhang Congcong1,Shi Yang1,Li Qing1,Li Na1,Mi Yong1

Affiliation:

1. Jinan Stomatological Hospital, 101 Jingliu Road, Jinan 250001, Shandong, China

Abstract

Background: Oral squamous cell carcinoma (OSCC) has been the sixth most common cancer worldwide. Emerging studies showed long non-coding RNAs to play a key role in human cancers. However, the molecular mechanisms underlying the initiation and progression of OSCC remained to be further explored. Objective: The present study aimed to identify differentially expressed lncRNAs and mRNAs in OSCC. Methods: GSE30784 was analyzed to identify differentially expressed lncRNAs and mRNAs in OSCC. Protein-protein interaction network and co-expression network analyses were performed to reveal the potential roles of OSCC related mRNAs and lncRNAs. Results: In the present study, we identified 21 up-regulated lncRNAs and 54 down-regulated lncRNAs in OSCC progression. Next, we constructed a lncRNA related co-expression network in OSCC, which included 692 mRNAs and 2193 edges. Bioinformatics analysis showed that lncRNAs were widely co-expressed with regulating type I interferon signaling pathway, extracellular matrix organization, collagen catabolic process, immune response, ECM-receptor interaction, Focal adhesion, and PI3K-Akt signaling pathway. A key network, including lncRNA C5orf66-AS1, C21orf15, LOC100506098, PCBP1-AS1, LOC284825, OR7E14P, HCG22, and FLG-AS1, was found to be involved in the regulation of immune response to tumor cell, Golgi calcium ion transport, negative regulation of vitamin D receptor signaling pathway, and glycerol- 3-phosphate catabolic process. Moreover, we found higher expressions of CYP4F29P, PCBP1- AS1, HCG22, and C5orf66-AS1, which were associated with shorter overall survival time in OSCC samples. Conclusions: Our analysis can provide novel insights to explore the potential mechanisms underlying OSCC progression.

Publisher

Bentham Science Publishers Ltd.

Subject

Computational Mathematics,Genetics,Molecular Biology,Biochemistry

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3