Background
Esophageal cancer (EC) is one of the deadliest cancers worldwide. Circular RNAs (circRNAs) have been implicated in the regulation of multiple human diseases, including cancer. In particular, the dysregulation of circRNA-0008717 has been linked to multiple types of cancer. However, the clinical significance and the molecular mechanisms of circRNA-0008717 in EC need to be further investigated. Therefore, this study aimed to prove the role of circRNA-0008717 in EC and its underlying molecular mechanism of action.
Conclusions
The proliferation, invasion, and migration of EC cells were enhanced by circRNA-0008717 sponging the miR-203 to increase Slug expression.
Methods
The expression of circRNA-0008717, miR-203, and the Slug was measured in two EC cell lines (EC109 and KYSE-150) by qRT-RCR. EC109 and KYSE-150 cells were first transfected with circRNA-0008717 siRNA (si-circRNA). After that, the proliferation, apoptosis, migration, and invasion of EC109 and KYSE-150 cells were measured. The western blot detected Slug, Vimentin, and E-cadherin protein levels. A dual-luciferase reporter gene assay was used to set up the interactions among circRNA-0008717, miR-203, and Slug.
Results
circRNA-0008717 expression was significantly upregulated in EC cells, and miR-2031 expression was decreased. Moreover, si-circRNA-0008717 or si-Slug inhibited the proliferation, migration, and invasion of EC cells. We found that circRNA-0008717 functioned as a sponge of miR-203, resulting in increased expression of Slug. We also reversed the effect of circRNA-0008717 knockdown on the EC progression by co-transfecting EC cells with a miR-203 inhibitor or Slug. Conclusions: The proliferation, invasion, and migration of EC cells were enhanced by circRNA-0008717 sponging the miR-203 to increase Slug expression.