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

<jats:title>Abstract</jats:title><jats:sec><jats:title>Background</jats:title><jats:p>Accumulated evidence has revealed that the dysregulation of micro ribonucleic acids (mi<jats:styled-content style="fixed-case">RNA</jats:styled-content>s) may contribute to esophageal squamous cell carcinoma (<jats:styled-content style="fixed-case">ESCC</jats:styled-content>). Mi<jats:styled-content style="fixed-case">R</jats:styled-content>‐93, which is a member of the mi<jats:styled-content style="fixed-case">RNA</jats:styled-content> cluster mi<jats:styled-content style="fixed-case">R</jats:styled-content>‐106b∼25, has been widely studied for its tumor promoting effect on different types of cancers. However, our knowledge of mi<jats:styled-content style="fixed-case">R</jats:styled-content>‐93 function in <jats:styled-content style="fixed-case">ESCC</jats:styled-content> remains unclear.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>The expression levels of mi<jats:styled-content style="fixed-case">R</jats:styled-content>‐93 in <jats:styled-content style="fixed-case">ESCC</jats:styled-content> 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 <jats:styled-content style="fixed-case">EC109</jats:styled-content> cells. To determine the possible target gene of mi<jats:styled-content style="fixed-case">R</jats:styled-content>‐93, cell transfection, Western blot analysis and luciferase reporter gene assays were performed.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>A significant upregulation of mi<jats:styled-content style="fixed-case">R</jats:styled-content>‐93 expression in <jats:styled-content style="fixed-case">ESCC</jats:styled-content> tissues was determined, combined with a downregulation of the predicted target gene, disabled 2 (<jats:styled-content style="fixed-case">DAB2)</jats:styled-content>. The introduction of mi<jats:styled-content style="fixed-case">R</jats:styled-content>‐93 significantly promotes cell proliferation, cell cycle progression, and the metastatic capability of <jats:styled-content style="fixed-case">EC109</jats:styled-content> cells. By cell transfection and luciferase reporter assay, <jats:styled-content style="fixed-case">DAB2</jats:styled-content> was confirmed as a direct target of mi<jats:styled-content style="fixed-case">R</jats:styled-content>‐93. In addition, the knockdown of <jats:styled-content style="fixed-case">DAB2</jats:styled-content> by small interfering <jats:styled-content style="fixed-case">RNA</jats:styled-content> displayed a consentaneous phenocopy with miR‐93 overexpression in <jats:styled-content style="fixed-case">EC109</jats:styled-content> cells.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>Our results indicate that mi<jats:styled-content style="fixed-case">R</jats:styled-content>‐93 acts as a tumor promoter in <jats:styled-content style="fixed-case">ESCC</jats:styled-content>, and its promotion effects on <jats:styled-content style="fixed-case">ESCC</jats:styled-content> cell proliferation and migration depend largely upon <jats:styled-content style="fixed-case">DAB2</jats:styled-content> suppression.</jats:p></jats:sec>