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LncRNA SNHG3 is activated by E2F1 and promotes proliferation and migration of non‐small‐cell lung cancer cells through activating TGF‐β pathway and IL‐6/JAK2/STAT3 pathway
Author(s) -
Shi Jindong,
Li Jiannan,
Yang Shuang,
Hu Xiaoying,
Chen Jiajun,
Feng Jingjing,
Shi Tianyun,
He Yanchao,
Mei Zhoufang,
He Wei,
Xie Juan,
Li Shanqun,
Jie Zhijun,
Tu Shuiping
Publication year - 2020
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.29194
Subject(s) - cell growth , cancer research , e2f1 , biology , stat protein , downregulation and upregulation , transcription factor , small nucleolar rna , stat3 , signal transduction , long non coding rna , microbiology and biotechnology , gene , biochemistry
Recently, long noncoding RNAs (lncRNAs) have been widely reported to play pivotal roles in the regulation of human cancers. Although the oncogenic property of lncRNA small nucleolar RNA host gene 3 (SNHG3) has been revealed in a variety of cancers, functions and regulatory mechanism of SNHG3 in non‐small‐cell lung cancer (NSCLC) remain to be investigated. In this study, we detected the upregulated expression of SNHG3 in NSCLC tissues as well as cells through quantitative reverse‐transcription polymerase chain reaction (qRT‐PCR) analysis. Using Kaplan–Meier analysis, we determined that a high‐level of SNHG3 was associated with a low overall survival rate of patients with NSCLC. Through gain and loss of function experiments, we demonstrated that SNHG3 had a significantly positive effect on NSCLC cell proliferation and migration. Mechanistic investigations revealed that SNHG3 was a predicted direct transcriptional target of E2F1. We observed that the transcriptional activation of SNHG3 could be induced by E2F1. To explore the mechanism, rescue experiments were carried out, which revealed that the cotreatment with SB‐431542, JSI‐124, or JSI‐124 + SB‐431542 rescued the effects brought by the overexpression of SNHG3 on NSCLC cell proliferation, migration, and epithelial‐mesenchymal transition process. Our results suggested that E2F1 activated SNHG3 and promoted cell proliferation and migration in NSCLC via transforming growth factor‐β pathway and interleukin‐6/janus‐activated kinase 2/signal transducer and activator of transcription 3 pathway, which implied that SNHG3 may be a biomarker for the treatment of patients with NSCLC.