Upregulation of the Long Noncoding RNA SNHG3 Promotes Lung Adenocarcinoma Proliferation

Liang Liu,^1,2 Jianjiao Ni,¹ and Xinhong He

^2,3

Academic Editor: Stamatios E. Theocharis

Received15 Dec 2017

Revised11 Apr 2018

Accepted14 May 2018

Published22 Jul 2018

Abstract

Lung cancer is the leading cause of cancer-associated mortalities worldwide. Non-small-cell lung cancer (NSCLC) is the main reason for cancer-relevant death and constitutes 80% of lung cancer cases. Long noncoding RNAs (lncRNAs) have been found to be related to different kinds of cancer. Long noncoding RNAs played important roles in regulating the pathological and physiological processes of numerous cancers. To explore novel lung adenocarcinoma-associated lncRNAs, we analyzed the TCGA database and found that the lncRNA SNHG3 was significantly upregulated in lung adenocarcinoma. Bioinformatic analysis showed that SNHG3 may play key roles in regulating RNA splicing, tRNA processing, signal transduction, cell adhesion, transcription, and apoptosis. We also performed functional experiments to explore the roles of SNHG3 in lung adenocarcinoma cells. We found that SNHG3 promoted proliferation, cell cycle, and suppressed cell apoptosis of lung adenocarcinoma, suggesting that SNHG3 acted as an oncogene in lung adenocarcinoma. We believe that this study will provide a potential new therapeutic and prognostic target for lung adenocarcinoma.