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LncRNA SNHG17 regulates cell proliferation and invasion by targeting miR-338-3p/SOX4 axis in esophageal squamous cell
Wenhu Chen1,2, Lifang Wang2, Xiaoyan Li2
1Department of Cell Biology and Genetics, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, China.
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.
Insights
Small nucleolar RNA host gene 17 (SNHG17) promotes esophageal squamous cell carcinoma (ESCC) progression by sponging miR-338-3p and upregulating SOX4. Inhibiting SNHG17 suppressed ESCC cell growth and invasion.
Area of Science:
- Oncology
- Molecular Biology
- RNA Biology
Background:
- Small nucleolar RNA host gene 17 (SNHG17) is a long noncoding RNA implicated in various cancers.
- The role of SNHG17 in esophageal squamous cell carcinoma (ESCC) remains largely uncharacterized.
Purpose of the Study:
- To investigate the expression pattern and functional mechanisms of SNHG17 in ESCC.
- To explore SNHG17 as a potential therapeutic target for ESCC.
Main Methods:
- Quantitative real-time PCR to assess SNHG17 expression.
- In vitro and in vivo experiments involving SNHG17 knockdown.
- Bioinformatic analysis to predict miRNA interactions.
- Luciferase reporter assays to validate miRNA-target interactions.
Main Results:
- SNHG17 was significantly upregulated in ESCC tissues and cell lines.
- SNHG17 knockdown inhibited ESCC cell proliferation, invasion, and epithelial-mesenchymal transition (EMT).
- SNHG17 acted as a molecular sponge for miR-338-3p, leading to increased SOX4 expression.
Conclusions:
- SNHG17 promotes ESCC progression through the SNHG17/miR-338-3p/SOX4 axis.
- Targeting the SNHG17 pathway represents a potential therapeutic strategy for ESCC.
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