Abstract
Small nucleolar RNA host gene 17 (SNHG17), a novel functional long noncoding RNA, has been demonstrated to play an essential role in the oncogenesis of several tumors. However, for esophageal squamous cell carcinoma (ESCC) the expression pattern and detailed function of SNHG17 are largely unknown. Hence, we conducted this study to explore potential roles and underlying oncogenic mechanisms for SNHG17 in ESCC progression. Results demonstrated SNHG17 to be markedly upregulated in ESCC. Knockdown of SNHG17 significantly suppressed ESCC cell proliferation, invasion, and epithelial–mesenchymal transition in vitro and tumor growth in vivo. Online database software analysis found miR-338-3p to interact with SNHG17 with the level of miR-338-3p negatively correlated with SNHG17 levels in ESCC samples. Further, miR-338-3p was found to directly target SRY-box transcription factor 4 (SOX4) in ESCC cells. Mechanistic analysis suggested that SNHG17 acts as an endogenous “sponge” competing with miR-338-3p to regulate SOX4, thereby promoting tumor progression. These results suggest that these molecular interactions may be potential therapeutic targets for ESCC.
Highlights
Worldwide, esophageal cancer (EC) is one of the most prevalent types of malignancy [1]
RESULTS Long noncoding RNA (lncRNA) Small nucleolar RNA host gene 17 (SNHG17) is overexpressed in Esophageal squamous cell carcinoma (ESCC) tissues and cells To investigate the effect of SNHG17 in ESCC, we analyzed high throughput sequencing data that compared the expression of SNHG17 in seven pairs of tissues from the GEO data set (GSE111011) and found SNHG17 expression to be upregulated in ESCC samples (Fig. 1A)
We assessed the expression of SNHG17 in ESCC based on TCGA data from the StarBase database and found SNHG17 to be upregulated in ESCC tissues compared to normal esophageal tissues (Fig. 1B)
Summary
Esophageal cancer (EC) is one of the most prevalent types of malignancy [1]. In this manner, it will be possible to develop more effective and precise treatments for this malignancy. The mechanism of action for lncRNAs has been described in a novel post-transcriptional regulation model In this model lncRNAs competitively sponge microRNAs and shield their target mRNAs, acting as competitive endogenous RNAs (ceRNAs) that neutralize their targets [13, 14]. Another lncRNA, MIR31HG, is highly expressed in pancreatic ductal adenocarcinoma, affecting cell proliferation and invasion by directly interacting with miR-193b [15]. Even though many lncRNAs have been confirmed involvement of tumorigenesis and progression, their biological role and potential mechanism of action in ESCC are not known
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