Circular RNA AKT3 governs malignant behaviors of esophageal cancer cells by sponging miR-17-5p

Abstract

Recent studies have demonstrated that circular RNA AKT3 (circAKT3) plays a crucial role in regulating the malignant phenotypes of tumor cells. However, the potential effects of circAKT3 on esophageal cancer have not been investigated. To illuminate the role of circAKT3 in malignant behaviors of esophageal cancer cells and its underlying mechanism. Clinical samples were collected to detect the expression of circAKT3. The role of circAKT3 in proliferation, migration, invasion, and apoptosis of esophageal cancer cells was evaluated using Cell Counting Kit-8, wound healing assays, Transwell assays, and fluorescence analysis, respectively. The target of circAKT3 was screened and identified using an online database and luciferase reporter assay. A xenograft nude mouse model was established to investigate the role of circAKT3 in vivo. In vitro assays showed that proliferative, migratory, and invasive capacities of esophageal cancer cells were significantly enhanced by circAKT3 overexpression. Furthermore, miR-17-5p was screened as the target of circAKT3, and miR-17-5p antagonized the effects of circAKT3 on esophageal cancer cells. Moreover, we identified RHOC and STAT3 as the direct target molecules of miR-17-5p, and circAKT3 facilitated expression of RHOC and STAT3 by inhibiting miR-17-5p. In vivo assays showed circAKT3 knockdown inhibited growth of esophageal cancer. CircAKT3 contributed to the malignant behaviors of esophageal cancer in vitro and in vivo by sponging miR-17-5p thus providing a potential target for treatment of esophageal cancer.