SNHG16/miR-140-5p axis promotes esophagus cancer cell proliferation, migration and EMT formation through regulating ZEB1

被引:77
作者
Zhang, Kai [1 ]
Chen, Jing [1 ]
Song, Haizhu [1 ]
Chen, Long-Bang [1 ]
机构
[1] Nanjing Univ, Sch Med, Jinling Hosp, Dept Med Oncol, Nanjing, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
esophagus cancer; long non-coding RNA; SNHG16; proliferation; EMT; LONG NONCODING RNA; MESENCHYMAL TRANSITION; POOR-PROGNOSIS; CARCINOMA; METASTASIS; INVASION; OSTEOSARCOMA; EXPRESSION; SNHG16;
D O I
10.18632/oncotarget.23178
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Esophageal squamous cell carcinoma (ESCC) is one of the most aggressive malignancies. Long noncoding RNAs (lncRNAs) have been identified to be associated with many diseases including tumors, and involved in the regulation of a wide array of pathophysiological processes. Small nucleolar RNA host gene 16 (SNHG16), also known as noncoding RNA expressed in aggressive neuroblastoma, was newly identified as a potential oncogene in many cancers. However, its role in ESCC has not been investigated. In the current study, the level of SNHG16 in the ESCC tissues and cell lines was measured by quantitative real-time PCR (qRT-PCR). Then loss-of-function assays were performed to explore the biological effects of SNHG16 in ESCC cell. Based on the online database analysis tools, we uncovered that miR-1405p could interact with SNHG16 and the level of miR-140-5p was inverse correlated with SNHG16 in ESCC specimens. Moreover, RIP, RNA pulldown system and dual luciferase reporter assay further provided evidence that SNHG16 directly targets miR140-5p by binding with microRNA binding site harboring in the SNHG16 sequence. Furthermore, bioinformatics analysis revealed that ZEB1 is a target of miR-140-5p in ESCC. Collectively, our findings suggested that SNHG16 could act as an oncogenic lncRNA that promotes tumor progression through acting as an endogenous 'sponge' by competing with miR-140-5p, thereby regulating target ZEB1.
引用
收藏
页码:1028 / 1040
页数:13
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