Micro ribonucleic acid‐93 promotes proliferation and migration of esophageal squamous cell carcinoma by targeting disabled 2
Chang Li1 
Cheng Ding1 
Tengfei Chen1 
Jun Chen1 
Zhenlei Xu1 
Zhe Lei2 
Chun Xu1 
[1] Department of Thoracic and Cardiovascular Surgery, The First Affiliated Hospital of Soochow University, Medical College of Soochow University, Suzhou, China;Soochow University Laboratory of Cancer Molecular Genetics, Medical College of Soochow University, Suzhou, China
Accumulated evidence has revealed that the dysregulation of micro ribonucleic acids (miRNAs) may contribute to esophageal squamous cell carcinoma (ESCC). MiR-93, which is a member of the miRNA cluster miR-106b∼25, has been widely studied for its tumor promoting effect on different types of cancers. However, our knowledge of miR-93 function in ESCC remains unclear.
Methods
The expression levels of miR-93 in ESCC and the adjacent non-tumor tissues were measured by real-time polymerase chain reaction. Cell counting kit-8, flow cytometry, and 5-ethynyl-2′-deoxyuridine incorporation and transwell migration assays were employed to explore the effects of miR-93 on proliferation and migration capabilities in EC109 cells. To determine the possible target gene of miR-93, cell transfection, Western blot analysis and luciferase reporter gene assays were performed.
Results
A significant upregulation of miR-93 expression in ESCC tissues was determined, combined with a downregulation of the predicted target gene, disabled 2 (DAB2). The introduction of miR-93 significantly promotes cell proliferation, cell cycle progression, and the metastatic capability of EC109 cells. By cell transfection and luciferase reporter assay, DAB2 was confirmed as a direct target of miR-93. In addition, the knockdown of DAB2 by small interfering RNA displayed a consentaneous phenocopy with miR-93 overexpression in EC109 cells.
Conclusion
Our results indicate that miR-93 acts as a tumor promoter in ESCC, and its promotion effects on ESCC cell proliferation and migration depend largely upon DAB2 suppression.
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