LncRNA SNHG17 regulates cell proliferation and invasion by targeting miR-338-3p/SOX4 axis in esophageal squamous cell carcinoma

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作者
Wenhu Chen
Lifang Wang
Xiaoyan Li
Changan Zhao
Liang Shi
Hongguang Zhao
Chen Huang
机构
[1] Xi’an Jiaotong University Health Science Center,Department of Cell Biology and Genetics, School of Basic Medical Sciences
[2] Hangzhou Medical College,School of Basic Medical Sciences & Forensic Medicine
[3] Xi’an Jiaotong University Health Science Center,Department of Pathology, School of Basic Medical Sciences
[4] Zhejiang Cancer Hospital,Department of Ward Pharmacy
[5] Zhejiang Cancer Hospital,Department of Thoracic surgery
[6] Xi’an Jiaotong University Health Science Center,Key Laboratory of Environment and Genes Related to Diseases
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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.
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