Research Papers:

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

Kai Zhang, Jing Chen, Haizhu Song and Long-Bang Chen _

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Oncotarget. 2018; 9:1028-1040. https://doi.org/10.18632/oncotarget.23178

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Kai Zhang1,*, Jing Chen1,*, Haizhu Song1 and Long-Bang Chen1

1Department of Medical Oncology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, Jiangsu, China

*These authors have contributed equally to this work

Correspondence to:

Long-Bang Chen, email: [email protected]

Keywords: esophagus cancer; long non-coding RNA; SNHG16; proliferation; EMT

Received: July 25, 2017     Accepted: November 26, 2017     Published: December 11, 2017


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-140-5p 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 miR-140-5p 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.

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