Abstract
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.
Highlights
Gastric cancer (GC) is one of the most common digestive malignant tumors and ranks as the second cause of death by malignancy worldwide [1, 2]
The results showed that the expression of small nucleolar RNA host gene 20 (SNHG20) in three human gastric cancer (GC) cells were significantly up-regulated compared with normal gastric epithelial cell GES-1 (Figure 1A)
To further detected the biological function of SNHG20 in GC progression, we knocked down SNHG20 in MKN45 or BGC-823 cells by using three siRNAs oligos (Figure 1B–1C), and overexpressed the SNHG20 levels by transfecting pcDNA3.1SNHG20 into BGC-823 cells (Figure 1D).The results showed that the SNHG20 was effectively inhibited by si-SNHG20-2, and the si-SNHG20-2 was used in the following study
Summary
Gastric cancer (GC) is one of the most common digestive malignant tumors and ranks as the second cause of death by malignancy worldwide [1, 2]. An improved understanding of molecular biology mechanisms involved in gastric cancer progression will facilitate the development of effective targeted therapeutic strategies for patients. Long non-coding RNAs (LncRNAs) have attracted much attention in cancer research field and act as key regulators of cellular development, proliferation, differentiation and apoptosis. Kong et al found long non-coding RNA PVT1 indicated a poor prognosis in gastric cancer patients and promoted GC cell proliferation through epigenetically regulating p15 and p16 expression [8]. Zhao et al reported that long non-coding RNA Linc00152 was involved in cell cycle arrest, apoptosis, epithelial to mesenchymal transition, cell migration and invasion in gastric cancer [9]. Aberrant expression of MALAT1 was confirmed to bind EZH2, suppressed the tumor suppressor PCDH10, and promoted gastric cancer cell migration and invasion [10]
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