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Micro ribonucleic acid-93 promotes proliferation and migration of esophageal squamous cell carcinoma by targeting disabled 2

BACKGROUND: 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...

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Detalles Bibliográficos
Autores principales: Li, Chang, Ding, Cheng, Chen, Tengfei, Chen, Jun, Xu, Zhenlei, Lei, Zhe, Xu, Chun, Zhao, Jun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley & Sons, Ltd 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4511333/
https://www.ncbi.nlm.nih.gov/pubmed/26273410
http://dx.doi.org/10.1111/1759-7714.12242
Descripción
Sumario:BACKGROUND: 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.