Research Papers:

Long noncoding RNA SNHG20 promotes gastric cancer progression by inhibiting p21 expression and regulating the GSK-3β/β-catenin signaling pathway

Jie Liu, Lanyu Liu, Jin-Xiang Wan _ and Ying Song

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Oncotarget. 2017; 8:80700-80708. https://doi.org/10.18632/oncotarget.20959

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Jie Liu1,*, Lanyu Liu2,*, Jin-Xiang Wan3 and Ying Song4

1Department of Intensive Care Unit, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei, China

2Department of Gynecology and Obstetrics, Weifang Hospital of Maternal and Child Health, Weifang, Shandong Province, China

3Department of Medical Ultrasonics, Huai'an Second People's Hospital, The Affiliated Huai'an Hospital of Xuzhou Medical University, Huai'an, China

4Department of Outpatient, People’s Hospital of Zoucheng, Zoucheng, China

*Co-first authors

Correspondence to:

Jin-Xiang Wan, email: [email protected]

Ying Song, email: [email protected]

Keywords: gastric cancer, small nucleolar RNA host gene 20, EZH2, p21

Received: July 29, 2017     Accepted: August 24, 2017     Published: September 16, 2017


Recent studies have indicated that long non-coding RNAs (lncRNAs) play important regulatory roles in tumor development and progression. However, the contribution of small nucleolar RNA host gene 20 (SNHG20) to gastric cancer development remains largely unknown. The aim of the study is to investigate the functional significance of SNHG20 involved in gastric cancer (GC) progression. In the study, our results demonstrated that the expression levels of SNHG20 were remarkably up-regulated in GC cells. Functionally, SNHG20 promoted the GC MKN45 and BGC-823 cells proliferation and invasion. Furthermore, knockdown of SNHG20 significantly inhibited the epithelial-mesenchymal transition (EMT) in MKN45 and BGC-823 cells, whereas, the overexpression of SNHG20 had the promoting effects. Moreover, we found that overexpression of SNHG20 in MKN45 and BGC-823 cells significantly inhibited the expression of E-cadherin and p21 via binding to EZH2 and regulated the GSK-3β/β-catenin signaling pathway. Thus, the results showed that SNHG20 acted as an oncogene in GC and targeting SNHG20 may serve as a therapeutic target for GC.

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